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Effects of Estrous Cycle and of in vivo Unilateral or Bilateral Adrenal Demedullation on the Distribution of Norepinephrine and Epinephrine Between Different Zones of the Adrenal
Abstract
The distribution of norepinephrine (NE) and epinephrine (E) between the capsule/glomerular zone and the remainder of the adrenal was studied in the adult female rat. Both catecholamines were present in these two parts of the gland. The concentration of E was higher than that of NE. In the capsule/glomerular zone the catecholamine concentrations were more than twenty to thirty times lower than in the inner part of the gland. The circulating levels of catecholamines were always very low. The present data also support very weak or no changes in catecholamine concentrations in both parts of the adrenal during the different stages of the estrous cycle.
The plasma levels of both aldosterone and corticosterone, like those of catecholamines, did not vary significantly throughout the estrous cycle. One week after unilateral or bilateral demedullation, both E content and concentration were reduced in the whole capsule/glomerular zone of the adrenal although the NE content did not change. The reduction of NE concentration could be related to the drastic weight increase of this part of the gland on the operated side. Moreover, unilateral demedullation was unable to significantly modify the plasma levels of both E and NE. In contrast bilateral demedullation suppressed circulating E and induced a significant reduction (about 50%) of NE plasma level. The present data suggest: 1) an extra-adrenal origin for the NE innervation of the capsule/glomerular zone of the adrenal cortex, and 2) a dual origin for E in the capsule/glomerular zone; part of E could arise from the adrenal medulla and part from an extra-adrenal site.
... For plasma samples, an alumina extraction procedure was employed to purify and concentrate the catecholamines they contained according the method previously described [14]. After extraction, a volume of 20 ml of acid supernatant containing catecholamines was then injected into the HPLC system coupled with electrochemical detection according to the method previously described [1]. ...
... For plasma samples, an alumina extraction procedure was employed to purify and concentrate the catecholamines they contained according the method previously described [14]. After extraction, a volume of 20 ml of acid supernatant containing catecholamines was then injected into the HPLC system coupled with electrochemical detection according to the method previously described [1]. ...
Autonomic dysreflexia (AD) occurs in up to 80% of quadriplegics and high paraplegics and is characterized by exaggerated sympathetic reflexes which induced paroxysmal hypertension. The aim of this study was to determine if plasma catecholamine levels increased during autonomic dysreflexia in the chronic spinal cord-injured (SCI) rats with special care to adrenaline. Catecholamine samples were collected before, during and 1 h after AD induced hypertension with colorectal distension. Results showed that plasma noradrenaline and adrenaline levels increased respectively 1.5-fold and 5-fold during AD in the chronic SCI rats. This suggests substantial roles for these two hormones in mediating the cardiovascular changes during AD. Knowledge of catecholamine levels during AD may thus aid in determining pathophysiology and potential pharmacologic treatments of this autonomic dysfunction.
The effects of glucocorticoids on adrenal neuropeptide Y (NPY) and NPY mRNA levels have been investigated on adult male rats of the Wistar strain subcutaneously injected twice a day with dexamethasone (5 mg/day), metyrapone (66 mg/day) or solvent (NaCl 0.9%) for 2.5 days and sacrificed 2 h after the last injection. Dexamethasone induced a significant decrease in both the adrenal weight (30%) and the plasma corticosterone concentration (85 %) but a significant increase of the adrenal NPY content (about 25%) as well as of its mRNA (0.8 kb) (>100%), revealed by Northern blot analysis and by in situ hybridization. Dexamethasone was unable to affect significantly dopamine (DA), norepinephrine (NE) and epinephrine (E) content of the adrenals; in contrast, it induced a significant decrease (30%) of the plasma NE level. Metyrapone elicited a drop of the plasma corticosterone level (80%), but a rise (near 150%) of the plasma ACTH concentration associated with an increase (19%) of the adrenal weight, a significant increase (30%) in the amount of adrenal NPY as well as a rise (>200%) of NPY mRNA content of the adrenal. Such treatment increased DA and NE (40%), and decreased E (>30%) content of the adrenals. Metyrapone-induced changes of catecholamine concentrations in the plasma were similar to that observed in the adrenal gland. Data suggest that the increase in adrenal NPY mRNA content induced by dexamethasone is more likely due to humoral effect rather than nervous effect of this synthetic glucocorticoid on the adrenal medulla. A neural mechanism as splanchnic nerve activation in response to severe corticosterone deficiency is a reasonable hypothesis to explain the increase in adrenal NPY mRNA induced by metyrapone, although there are probably other, nonneural mechanisms by which metyrapone could stimulate adrenal NPY. Present data are consistent with glucocorticoid regulation of NPY gene expression and/or steady-state level of NPY mRNA in the adrenal gland.
The Yucatan Peninsula nesting hawksbill turtles' population (Eretmochelys imbricata Linnaeus 1766) is the biggest in the Caribbean and fourth in the world; within the Ria Lagartos Biosphere Reserve, at El Cuyo beach both hawksbill and green turtle (Chelonia mydas Linnaeus 1754) nest. In the present study, the nesting trend and reproductive output of both species during three consecutive nesting seasons (2002-2004) was evaluated. Night patrols from mid April to September allowed the collection of data on number of nests, nest location and size of females. The number of hawksbill and green turtles' nests decreased along these seasons. No differences were found in mean length of female turtles of both species between nesting seasons. Both species showed high nest site fidelity with average distance between nests of 3 km for Hawksbill and 1.8 km for Green turtles. The regression analysis between size and fecundity was significant (p < 0.05) for both species. The spatial variation of laid nests was also analyzed revealing that both species nested mainly on the dune zone. Predation has risen on El Cuyo beach, affecting mostly hawksbills nests. Hurricane Ivan destroyed the majority of green turtles nests in 2004.
The present investigation concerns 80–90 day-old male rats born from morphine-exposed mothers (2×10 mg/kg per day from days 11 to 18 of gestation which showed at birth reduced size and activity of the adrenals). This prenatal treatment did not significantly disturb under resting conditions: (1) the postnatal body growth up to week 10 after birth, (2) the activity of the pituitary gonadal axis (circulating luteinizing hormone (LH) and testosterone (T), weight of the testicles and seminal vesicles), (3) the activity of the hypothalamo-pituitary-adrenal axis (HPA) (hypothalamic corticoliberin (CRF) content, plasma adrenocorticotrophic hormone (ACTH) level, adrenal weight and corticosterone (B) content, plasma B level) as well as Bmax and Kd of mineralocorticoid (type I) and glucocorticoid (type II) receptors to B in both the hippocampus and the hypothalamus. In contrast these rats showed reduced content of adrenals in noradrenaline (NA) and adrenaline (A) but increased circulating levels of A.
The effects of neuropeptide Y (NPY1-36), of two analogs (Leu31-Pro34 NPY and NPY18-36) and of Peptide YY (PYY) on aldosterone and corticosterone secretions by freshly isolated rat adrenal capsule/zona glomerulosa preparations were investigated in vitro. NPY-related peptides (NPY1-36, Leu31-Pro34 NPY, NPY18-36), but not PYY, induced a dose-dependent release of aldosterone at concentrations ranging from 10(-8) to 10(-6) M. All the investigated peptides failed to significantly affect corticosterone secretion in concentrations ranging from 10(-10) to 10(-6) M (NPY1-36, NPY18-36), 10(-11) to 10(-6) M (Leu31-Pro34 NPY) or 10(-9) to 10(-6) M (PYY). Aldosterone secretion by this preparation of isolated adrenal capsule/zona glomerulosa was also significantly stimulated by high potassium levels (55 mEq) or by angiotensin II (AII) in concentrations ranging from 10(-8) to 10(-6) M. Moreover, NPY and Y1 or Y2 receptor agonists were positive aldosterone releasing agents as potent as AII. The present data support the existence of: (1) NPY binding sites of the Y3-like subtype, on rat adrenal capsule/zona glomerulosa. (2) A stimulatory effect of NPY on aldosterone production. So that the NPYergic innervation of the rat adrenal capsule/zona glomerulosa could be implicated in the multifactorial control of aldosterone production.
The effects of two Neuropeptide Y (NPY) analogs (Y1- and Y2-type) and vasoactive intestinal peptide (VIP) on both catecholamine (adrenaline and noradrenaline) release and aldosterone production by rat adrenal capsule/glomerular zone, have been investigated in vitro. The adrenal capsule/glomerular zones, collected from adult male rats, were incubated in a medium (Krebs-Ringer bicarbonate buffer supplemented with glucose and bovine serum albumin) containing or not one of the following synthetic peptides: human Leu31,Pro34-NPY (an agonist of the Y1-type receptors), human/porcine NPY18-36 (an agonist of the Y2-type receptors) and VIP at the concentration of 10(-7) M, associated or not with 10(-7) M atenolol (a beta 1 adrenergic antagonist) or ICI-118,551 hydrochloride (a beta 2 adrenergic antagonist). The two NPY analogs as well as the VIP stimulated the release of catecholamines and of aldosterone. The beta 1 adrenergic antagonist, but not the beta 2 one, which failed to affect basal aldosterone production when given alone, prevented NPY18-36-, Leu31,Pro34-NPY- or VlP-induced aldosterone secretion. Present data support the hypothesis that adrenaline and/or noradrenaline could mediate the effects of both NPY and VIP on aldosterone secretion via beta 1 adrenergic receptors; alternatively, the steroidogenic effect of NPY or VIP could be related to direct interaction between NPY- or VIP-specific binding sites, present on the capsule/glomerular zone of the rat adrenal cortex, and beta 1 adrenergic receptors. Then the NPYergic, VIPergic and catecholaminergic innervation of the adrenal cortex, previously characterized by immunohistochemistry, may be a potent stimulatory element in the nervous control of the aldosterone secretion.
The capsule/glomerulosa zone of the adrenal gland is richly innervated by neuropeptide Y (NPY)-containing nerve fibers. The content and concentration of NPY in the capsule/glomerulosa zone of the female rat adrenal were determined by radioimmunoassay both in unoperated females (controls) and in operated ones, a week after in situ unilateral demedullation which excludes both the medulla and the fasciculata/reticularis zones. Demedullation induced a significant weight increase of the capsule/glomerulosa zone of the operated gland (compared to contralateral intact one) as well as of the medulla/fasciculata-reticularis zone of the contralateral intact one (compared to the corresponding part of the gland of controls). Both NPY content and concentration in the capsule/glomerulosa zone of the demedullated adrenal were significantly reduced in comparison with those in the corresponding part of the contralateral intact gland. NPY immunoreactive fibers, revealed by immunofluorescence, were present in the capsule/glomerular zone of both intact and contralateral demedullated adrenal gland. In the former, NPY fibers were regularly distributed in this part of the gland, while in the latter, some areas were devoid of immunoreactive fibers. NPY content, but not concentration, was increased in the medulla/fasciculata-reticularis zone of the contralateral intact gland. Present data support a dual origin for the NPY nerves present in the capsule/glomerulosa zone of the adrenal cortex: one part could arise from extra-adrenal site possibly the suprarenal ganglia while the other part could arise from intra adrenal ganglia cells which also contain NPY.
It is noteworthy that in the rat the early postnatal life is marked by an activation of both the corticostimulating function of the adenohypophysis in neonates of both sexes and of the gonadostimulating function mainly in males. In order to specify if such neuroendocrine variations are temporally correlated with changes in the hypothalamic metabolism of neurotransmitters, the hypothalamic metabolism of serotonin (5 HT), norepinephrine (NE), and dopamine (DA) and the hypothalamic content of neuropeptide Y (NPY) have been investigated in newborn rats of both sexes, delivered at term by cesarean section, as well as changes in the activity of both the hypothalamo-pituitary adrenal axis (HPA) and the hypothalamo-pituitary gonadal axis (HPG). Experimental data suggested that 1) in males a rise in hypothalamic metabolism of 5 HT, NE and DA occurs during the first two hours after delivery, whereas in females, only the metabolism of NE increases. Moreover, the postnatal metabolism of NE was higher in females than in littermate males; 2) NPY content of the hypothalamus, which was at birth significantly higher in males than in females, dropped in the former but not in the latter; 3) in newborn males, an early surge of plasma testosterone occurs, suggesting postnatal activation of the HPG axis; on the other hand, in females, a late and slight increase in plasma estradiol is observed; 4) in early postnatal life, a sex-independent rise in plasma ACTH and adrenal and plasma corticosterone levels suggest a comparable activation of the HPA axis in newborns of both sexes. In conclusion, the early postnatal activation of the corticostimulating function in neonates of both sexes and that of the gonadostimulating function, mainly in males, could be temporally correlated with a rise in the hypothalamic metabolism of two neurotransmitters, 5 HT and NE, and of NPY content. According to our data, a sex-dependent metabolism of neurotransmitters in the hypothalamus is already apparent in early postnatal life.
Catecholamines and neuropeptide Y (NPY) levels were determined in the adrenals of rats treated for 2.5 days with chlorisondamine (6 mg/day), a nicotinic ganglionic blocking agent, metyrapone (66 mg/day), an inhibitor of the 11 beta-hydroxylase activity or both metyrapone and chlorisondamine. Chlorisondamine induced a significant increase in adrenal weight (31%) without significant rise in hypothalamic CRH content, plasma ACTH level and plasma corticosterone concentration. This drug was unable to affect significantly dopamine (DA), norepinephrine (NE) and epinephrine (E) content of the adrenals; in contrast, it induced a significant decrease (90%) of plasma NE and E levels. Chlorisondamine induced no change in adrenal NPY content as well as NPY mRNA level determined by Northern blot but significantly increased NPY plasma level. Metyrapone-treatment induced a significant drop of plasma corticosterone level and elicited a significant reduction of hypothalamic CRH content, a rise (460%) of the plasma ACTH concentration associated with a significant increase (18%) of the adrenal weight. A marked increase of DA (240%) and significant decrease of E (22%) in the adrenal gland were observed in response to metyrapone treatment. In addition, metyrapone induced a drop (23%) in plasma E level. In both the adrenals and the plasma, the ratio E/NE was significantly reduced by metyrapone treatment. Metyrapone elicited a significant increase of adrenal NPY content (88%) as well as of NPY mRNA revealed by Northern blot analysis but was unable to significantly affect NPY plasma level. The effects of chlorisondamine, given in combination with metyrapone on both hypothalamic CRH content and plasma ACTH level, were similar to those induced by metyrapone given alone. Chlorisondamine-mediated pharmacological ganglionic blockade increased metyrapone-induced adrenal hypertrophy and adrenal DA storage but prevented metyrapone-induced depletion of adrenal E as well as increase of the adrenal NPY mRNA level and NPY content. Chlorisondamine-induced elevation of plasma NPY level was not observed under metyrapone treatment. Present data suggest that the increase in adrenal NPY synthesis in response to metyrapone treatment is mediated by transsynaptic cholinergic activation and implies nicotinic receptors. On the other hand, adrenal TH may be regulated by additional or different mechanisms, which possibly involve nonnicotinic transmission. Present work also suggests that the suppression of the glucocorticoid feedback inhibition of hypothalamic CRH neurons could stimulate sympathoneuronal outflow and consequently elicit transsynaptic cholinergic activation of adrenal neuropeptide Y gene expression.
Neuropeptide Y (NPY) is found in cell bodies of neurons in the brain and co-localized with noradrenaline (NA) in sympathetic nerves as well as with NA and adrenaline (A) in the adrenal chromaffin cells. The purpose of the present work is to determine whether NPY and catecholamines found in the plasma of the rat under resting and stress conditions (ether inhalation, restraint) arise from the adrenals or from extra-adrenal sites. We used adrenalectomized (adx) rats and sham-adx ones. Adrenalectomy increased plasma adrenocorticotrophic hormone (ACTH) levels but decreased drastically circulating corticosterone (B) and A (-97%). However, resting NA was slightly but not significantly decreased and NPY not affected. Ether inhalation (3 min) increased plasma levels of ACTH, B, NA and A in sham-adx rats, ACTH, NA and, weakly, A in adx ones. Restraint (30 min) increased B, NA and A in sham-adx rats, NA and, poorly, A, in adx ones. In contrast, plasma levels of NPY were not significantly affected by these stress conditions. The present data suggest that NA found in rat plasma at rest and during ether or restraint stress could arise from both adrenal medulla and noradrenergic nerve endings while A arises mainly from the adrenergic chromaffin cells of the adrenals. In contrast, NPY found in the circulation, at rest and under stress conditions, is not derived from the adrenals but emanates mainly from an extra-adrenal source.
Exposure of pregnant rats to morphine, from day 11 to day 18 of gestation, was previously reported to induce both an adrenal atrophy and hypoactivity of the glucocorticoid function in newborns at term, but did not affect, in vitro, the responsiveness of those glands to adrenocorticotrophin hormone (ACTH) concerning corticosterone release. Moreover, these effects were mediated by maternal hormones from the adrenal glands. In the present work, we investigated the effects of a prenatal morphine exposure on the mineralocorticoid activity of the adrenals in neonates. The first aim of the present study was to determine in these newborns 1) the adrenal and plasma aldosterone concentrations at birth time and during the early postnatal period 2) the plasma levels of Na+ and K+ at birth time, 3) the in vitro responsiveness of the newborn adrenals to angiotensin II (A(II)) and ACTH. The second aim of our study was to investigate the mineralocorticoid activity of the adrenals in newborns from adrenalectomized mothers treated with morphine during gestation. According to present data morphine given to intact mothers induced in newborns a severe adrenal atrophy but increased adrenal aldosterone content and plasma aldosterone level. However, prenatal morphine was unable to affect significantly Na+/K+ ratio in both mothers and newborns. In vitro, the adrenals of neonates from morphine-treated mothers were unresponsive to An and ACTH for promoting aldosterone release; in contrast, aldosterone secretion was significantly stimulated by high potassium levels (55 mEq). Maternal adrenalectomy performed one day before the beginning of morphine treatment prevented morphine-induced adrenal atrophy but was unable to affect significantly the adrenal mineralocorticoid function of the offspring. Such data suggest that a prenatal morphine exposure stimulated both aldosterone synthesis and release in neonates. However, this basal hyperfunction did not appear to be coupled with an enhanced adrenal responsivity to AII or ACTH. Prenatal morphine-induced hyperactivity of the mineralocorticoid function of the newborn adrenals, which drastically contrast with hypoactivity of the glucocorticoid one, was independent of adrenal factors from maternal origin.
Gabolysat PC60 is a fish protein hydrolysate with anxiolytic properties commonly used as a nutritional supplement.
The diazepam-like effects of PC60 on stress responsiveness of the rat pituitary-adrenal system and on sympathoadrenal activity were studied.
The activity of the pituitary-adrenal axis, measured by plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone (B) of the sympathoadrenal complex, measured by circulating levels of noradrenaline (NA) and adrenaline (A), and the gamma aminobutyric acid (GABA) content in the hippocampus and the hypothalamus were investigated in male rats which received daily, by an intragastric feeding tube, for 5 days running either diazepam (1 mg/kg) or PC60 (300 or 1,200 mg/kg). Controls received only solvent (carboxymethylcellulose 1%). Six hours after the last force-feeding, the rats were subjected to 3 min ether inhalation or 30 min restraint and killed by decapitation 30 min after ether stress or at the end of restraint.
Baseline plasma levels of ACTH, B, NA and A were not affected by either diazepam or PC60. Both ether- and restraint-induced release of ACTH, but not B, were similarly and drastically reduced by diazepam and PC60 (1,200 mg/kg). Both diazepam and PC60 (1,200 mg/kg) deleted restraint-induced NA and A increases. Both treatments also reduced the ether-induced rise of A. Basal levels of GABA were significantly increased in both the hippocampus and the hypothalamus in PC60-treated rats and only in the hippocampus in diazepam-treated ones. In controls, ether inhalation as well as restraint increased GABA content of these two brain structures. In contrast, such stress procedures performed in PC60-treated rats reduced GABA content slightly in the hippocampus but significantly in the hypothalamus. In diazepam-treated rats, GABA content of the hypothalamus was unaffected by stresses but that of the hippocampus was slightly decreased.
Present data suggest diazepam-like effects of PC60 on stress responsiveness of the rat pituitary adrenal axis and the sympathoadrenal activity as well as GABA content of the hippocampus and the hypothalamus under resting and stress conditions. These effects of PC60 agree with anxiolytic properties of this nutritional supplement, previously reported in both rats and humans.
In humans, an altered control of cortisol secretion was reported in adult men born with a low birth weight making the hypothalamic-pituitary-adrenal (HPA) axis a possible primary target of early life programming. In rats, we have recently shown that maternal food restriction during late pregnancy induces both an intrauterine growth retardation and an overexposure of fetuses to maternal corticosterone, which disturb the development of the HPA axis in offspring. The first aim of this work was to investigate, in adult male rats, whether perinatal malnutrition has long-lasting effects on the HPA axis activity during both basal and stressful conditions. Moreover, as the HPA axis and sympathetic nervous system are both activated by stress, the second aim of this work was to investigate, in these rats, the adrenomedullary catecholaminergic system under basal and stressful conditions. This study was conducted on 4-month-old male rats malnourished during their perinatal life and on age-matched control animals. Under basal conditions, perinatal malnutrition reduced body weight and plasma corticosteroid-binding globulin (CBG) level but increased mineralocorticoid receptor (MR) gene expression in CA1 hippocampal area. After 30 min of restraint, perinatally malnourished (PM) rats showed increased plasma noradrenaline, adrenocorticotropin hormone (ACTH) and corticosterone concentrations similarly as controls, but calculated plasma-free corticosterone concentration was significantly higher and adrenaline level lower than controls. During the phase of recovery, PM rats showed a rapid return of plasma ACTH and corticosterone concentrations to baseline levels in comparison with controls. These data suggest that in PM rats, an elevation of basal concentrations of corticosterone, in face of reduced CBG and probably increased hippocampal MR lead to a much larger impact of corticosterone on target cells that mediate the negative-feedback mechanism on the activities of both the HPA axis and sympathoadrenal one.
The hypothalamic corticotropin-releasing hormone system and the sympathetic nervous system are anatomically and functionally interconnected and hormones of the hypothalamic-pituitary-adrenocortical axis contribute to the regulation of catecholaminergic systems. To investigate the role of glucocorticoids on activity of the adrenal gland, we analysed plasma and adrenal catecholamines, tyrosine hydroxylase (TH) and phenylethanolamine N-methyltransferase (PNMT) mRNA expression in rats injected with metyrapone or dexamethasone. Metyrapone-treated rats had significantly lower epinephrine and higher norepinephrine production than control rats. Metyrapone increased TH protein synthesis and TH mRNA expression whereas its administration did not affect PNMT mRNA expression. Dexamethasone restored plasma and adrenal epinephrine concentrations and increased PNMT mRNA levels, which is consistent with an absolute requirement of glucocorticoids for PNMT expression. Adrenal denervation completely abolished the metyrapone-induced TH mRNA expression. Blockage of cholinergic neurotransmission by nicotinic or muscarinic receptor antagonists did not prevent the metyrapone-induced rise in TH mRNA. Finally, pituitary adenylate cyclase activating polypeptide (PACAP) adrenal content was not affected by metyrapone. These results provide evidence that metyrapone-induced corticosterone depletion elicits transsynaptic TH activation, implying noncholinergic neurotransmission. This may involve neuropeptides other than PACAP.
The effects of a 3-day water deprivation were studied in adult female rats in order to know what are the different zones of the adrenal gland and the hormonal factors involved in the growth and the activity of the adrenal gland. Water deprivation significantly increased plasma renin activity (PRA), plasma Angiotensin II (AII), vasopressin (AVP), epinephrine, aldosterone and corticosterone concentrations but did not modify the plasma adrenocorticotropin hormone (ACTH) level. Water deprivation significantly increased the absolute weight of the adrenal capsule containing the zona glomerulosa without modification of the density of cells per area unit suggesting that the growth of the adrenal capsule was due to a cell hyperplasia of the zona glomerulosa. Water deprivation significantly increased the density of AII type 1 (AT(1)) receptors in the adrenal capsule but did not modify the density of AII type 2 (AT(2)) receptors in the adrenal capsule and core containing the zona fasciculata, the zona reticularis and the medulla. The treatment of dehydrated female rats with captopril, which inhibits the angiotensin converting enzyme (ACE) in order to block the production of AII, significantly decreased the absolute weight of the adrenal capsule, plasma aldosterone and the density of AT(1) receptors in the adrenal capsule. The concentration of corticosterone in the plasma, the density of AT(2) receptors and the density of cells per unit area in the zona glomerulosa of the adrenal capsule were not affected by captopril-treatment. In conclusion, these results suggest that AII seems to be the main factor involved in the stimulation of the growth and the secretion of aldosterone by the adrenal capsule containing the zona glomerulosa during water deprivation. The low level of plasma ACTH is not involved in the growth of the adrenal gland but is probably responsible for the secretion of corticosterone by the zona fasciculata.
Wistar rats have been selectively bred for high (HABs) or low (LABs) anxiety-related behavior based on results obtained in the elevated-plus maze. They also display robust behavioral differences in a variety of additional anxiety tests. The present study was undertaken to further characterize physiological substrates that contribute to the expression of this anxious trait. We report changes in brain and peripheral structures involved in the regulation of both the hypothalamo-pituitary-adrenal (HPA) and sympatho-adrenal systems. Following exposure to a mild stressor, HABs displayed a hyper-reactivity of the HPA axis associated with a hypo-reactivity of the sympatho-adrenal system and a lower serotonin turnover in the lateral septum and amygdala. At rest, HABs showed a higher adrenal weight and lower tyrosine hydroxylase and phenylethanolamine-N-methyltransferase mRNAs expression in their adrenals than LABs. In the anterior pituitary, HABs also exhibited increased proopiomelanocortin and decreased vasopressin V1b receptor mRNAs expression, whereas glucocorticoid receptor mRNA levels remained unchanged. These results indicate that the behavioral phenotype of HABs is associated with peripheral and central alterations of endocrine mechanisms involved in stress response regulation. Data are discussed in relation to coping strategies adopted to manage stressful situations. In conclusion, HABs can be considered as an useful model to study the etiology and pathophysiology of stress-related disorders and their neuroendocrine substrates.
This paper compares noradrenaline content in the different parts of the oviduct in rabbits receiving or not a dose of estradiol-17 beta 24 h before human chorionic gonadotropin (HCG) and killed 60 h post HCG. 3,4-Dihydroxyphenylalanine assays were carried out in the oviduct after aromatic L-amino acid decarboxylase was inhibited by m-hydroxybenzylhydrazine (NSD 1015) in the same experimental conditions. Pauerstein et al. (1974) have shown that an intramuscular injection of 250 micrograms of estradiol-17 beta in rabbits 24 h before intravenous injection of 100 IU of HCG delays ovum transport at the ampullary-isthmic junction. The extent of this noradrenergic innervation suggested that estradiol could act at least partially through the noradrenergic systems. Our results show that estradiol-17 beta increased oviduct weight by water retention without modifying either the tyrosine hydroxylase activity or the noradrenaline content in any part of the oviduct and that, consequently, the estrogen-induced "tube locking" of ova was not mediated through the noradrenergic processes.
The activity of phenylethanolamine N-methyltransferase, the enzyme that catalyzes the N-methylation of noradrenaline to form adrenaline, falls following hypophysectomy. Enzyme activity can be restored by injections of adrenocorticotropic hormone (ACTH) or of dexamethasone, a potent synthetic glucocorticoid. The effect of ACTH on the adrenaline-forming enzyme is not direct, but involves stimulation of the release of endogenous glucocorticoids from the adrenal cortex. These steroids then act to elevate the activity of the transferase, which is principally localized in the adrenal medulla. The stimulation by glucocorticoids of phenylethanolamine N-methyltransferase activity can be blocked by the concurrent administration of puromycin or actinomycin D. Glucocorticoids do not stimulate the activity of other adrenal enzymes involved in catecholamine biosynthesis or metabolism, such as tyrosine hydroxylase, catechol O-methyltransferase, or monoamine oxidase.
The morphology and physiology of the adrenal medulla are described, emphasizing the rat medulla as an experimental model. Current concepts are reviewed relating to the development of medullary cell lineages and to factors that affect synthesis, storage, and secretion of hormones in the adrenal medulla. The pathophysiological implications of adrenal medullary cells as a multimessenger system are discussed.
The structure of the suprarenal venous system of 25 human suprarenal glands has been studied. From a structural point of view, four portions of the suprarenal vein have been distinguished: the proximal section, the hilus section, the section of the prehilus collaterals, and the distal section. In the hilus section and the section of the prehilus collaterals, the structure of the tunica media is more complex. In the hilus section, spiral fibres are found besides the longitudinal muscle fibres. Three strata of fibres can be observed in the section of the prehilus collaterals at the point where these veins drain into the central vein: two longitudinal strata, external and internal, and a third intermediate stratum corresponding to the looped fibres. The spiral and looped fibres, on contracting, can function as a sphincter. The longitudinal fibres, by means of the traction they exert on the stroma and connective capsule of the suprarenal, increase the intraglandular pressure while decreasing the periglandular pressure. A sympathetic stimulus provokes an increase in the secretion of adrenalin, and, at the same time, a contraction of the muscle fibres of the suprarenal venous system. Under these conditions, the venous return makes use of the emissary veins; and in this way, the secreted adrenalin establishes a close contact with the cortico-suprarenal parenchyma.
The hypothesis that dopamine (DA) is involved in the control of aldosterone secretion is given some support by the finding of DA in the adrenal cortex of several species, but the source of this DA is not known. This study showed that the administration of L-dopa to intact rats or medullectomized rats caused a significant DA increase in the adrenal cortex. The DA increase in the cortex was more pronounced than in the medulla, coincident with higher L-dopa uptake by the cortical tissue. Tyrosine administration raised DA levels only in the medulla. Sympathectomy of the rat by 6-hydroxydopamine treatment did not affect DA basal levels in the cortex or the DA increase in this tissue after L-dopa injection. 3,4-Dihydroxyphenylacetic acid (DOPAC) is detectable in the adrenal cortex but not in the adrenal medulla, and DOPAC levels increased significantly after L-dopa, which indicates monoamine oxidase (MAO) activity within the adrenal cortex. Because 6-hydroxydopamine pretreatment did not alter DOPAC levels, cortical MAO may be located outside catecholaminergic neurons. The results established circulating L-dopa as a precursor for DA in the adrenal cortex of the rat. They also showed that tyrosine hydroxylase activity is absent from the adrenal cortex of this species.
L'innervation des glandes surrenales a une action directe sur l'axe hypothalamo-hypophyso-surrenalien et donc sur la liberation des glucocorticoides. Cette action est similaire a celle de l'ACTH. En fait ce mecanisme se deroule en trois etapes distinctes: 1) liberation de neurotransmetteurs; 2) mise en route de la secretion endocrine et paracrine; 3) mise en route des systemes enzymatiques
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The classical perspective of the adrenal gland has, in general, treated the cortex and medulla as functionally independent tissues which, by chance, are located together. Recent data challenge this outlook, and there is now evidence of regulatory mechanisms which are common to both the cortex and the medulla. There is, additionally, more evidence that the products of each of these tissues may influence the function of the other.
In mammals the arrangement of the adrenal gland is such that the adrenal cortex forms the outer part of the gland and totally encloses the medulla. Indeed, a close anatomical relationship, between the morphologically and functionally distinct steroid-secreting tissue and chromaffin tissue in the adrenal gland, is seen in most vertebrate groups. Why should these embryologically unrelated tissues be located together, and what is their functional link?
There is a wealth of experimental evidence to support the contention that these tissues have
The effects of nerve activation and of the catecholamines epinephrine and norepinephrine on adrenal corticosteroid release were investigated in intact isolated perfused pig adrenals with preserved nerve supply. To study the contact zones of medullary and cortical tissues, porcine adrenals were examined on the histological and ultrastructural levels. Splanchnic nerve activation stimulated in parallel the release of epinephrine (from a basal value of 0.31 +/- 0.11 to 8.13 +/- 0.60 microgram/min) and norepinephrine (from 0.76 +/- 0.68 to 12.94 +/- 3.58 micrograms/min) and the release of the corticosteroids cortisol (from 0.62 +/- 0.19 to 2.00 +/- 0.35 micrograms/min) and aldosterone (from 3.34 +/- 0.59 to 7.53 +/- 1.63 ng sigma in). Also, perfusion of the isolated adrenals with catecholamines provoked a significant release of the corticosteroids. Epinephrine (10(-6) M) stimulated the release of cortisol (from 0.59 +/- 0.31 to 2.66 +/- 0.34 micrograms/min) and aldosterone (from 2.12 +/- 0.42 to 4.68 +/- 0.92 ng/min). Norepinephrine (10(-6) M) stimulated the release of cortisol (from 0.26 +/- 0.07 to 1.28 +/- 0.10 micrograms/min) and aldosterone (from 1.28 +/- 0.37 to 3.57 +/- 0.80 ng/min). Using an immunostaining for synaptophysin, which is specific for neuroendocrine cells, chromaffin cells could be detected within all three zones of the adrenal cortex. The two endocrine tissues appear to be closely interwoven. On the ultrastructural level, medullary cells are in apposition to cortical cells, with close cellular contacts. These results show that the release of corticosteroids cortisol and aldosterone can be stimulated through the sympatho-adrenal system. Taking into consideration the close colocalization of cortical and medullary tissues, this stimulation may be mediated by chromaffin cells in a paracrine manner.
The present study applied the separated adrenal capsules of rats for wholemount immunocytochemistry and used tyrosine hydroxylase (TH) antibody as a marker for catecholamines. TH-immunoreactive nerve bundles without varicosities and fibers with varicosities were seen to run along or to encircle blood vessels entering the adrenal capsule from the outside, and then to run along a network of blood vessels in the intracapsular region. Also, the TH-immunoreactive nerve bundles and fibers were found to run along blood vessels in the subcapsular region. Some TH-immunoreactive nerve fibers and bundles with varicosities, unassociated with the blood vessels, were seen in the subcapsular region. In this region, TH-immunoreactive nerve fibers with varicosities were often seen to be closely associated with the cortical cells. Some TH-immunoreactive nerve fibers without varicosities were visible within the splanchnic nerve in the subcapsular region. The present study suggests that numerous catecholaminergic nerve fibers are associated with blood vessels forming a network in the superficial region of the rat adrenal gland.
After the surgical removal of one adrenal gland, the cortex of the remaining adrenal gland increases in size. This compensatory adrenal growth is characterized by increased weight and DNA content of the remaining adrenal 72 h after unilateral adrenalectomy. In these experiments, chemical sympathectomy prevented compensatory adrenal growth. In rats sympathectomized by neonatal injections of 6-hydroxydopamine or guanethidine and unilaterally adrenalectomized at 40 days of age, the compensatory increase in weight in the remaining gland was attenuated (relative to a vehicle-injected control group) and not accompanied by the usual increase in DNA content. Augmented RNA content was observed after unilateral adrenalectomy in sympathectomized as well as vehicle-injected animals; presumably this reflects increased steroidogenesis because, despite the loss of one adrenal, the rats maintained normal plasma corticosterone and aldosterone levels (relative to the sham-adrenalectomized group). The sympathectomy procedures themselves did not significantly alter adrenal weight, adrenal nucleic acid content, or plasma aldosterone relative to vehicle-injected control levels; however, plasma corticosterone levels were significantly reduced. We conclude that the sympathetic nervous system mediates the adrenal cortical cell proliferation that occurs after unilateral adrenalectomy.
The responsiveness of perifused adrenal glands removed from rats at various stages of gestation to similar immunological quantities (2 ng) of 'big' approximately equal to 30,000 mol wt), 'intermediate' (congruent to 13,000 mol wt) and 'little' (approximately equal to 4500 mol wt) ACTH isolated by gel filtration chromatography from an acid extract of pituitary glands of 21 day-old rat foetuses was determined. This immunological quantity failed to induce a maximal response of the foetal adrenals. Corticosterone was determined in the effluent perifusion by a radiocompetition assay. On days 17 and 19 of gestation, intermediate and little ACTH had, on a weight basis, the same corticosteroidogenic activity, but on day 21 the little was more potent than the intermediate form. The corticosterone release by these two forms of ACTH was log-dose dependent. The biological activity of big ACTH was very low on day 17, slightly increased until day 21 but remained significantly lower than that of intermediate and little forms. Big ACTH added to little ACTH in the perifusion medium did not modify the corticosteroidogenic activity of little ACTH on days 17, 19 and 21 of gestation.
Effect of adrenergic activity on the adrenal steroidogenesis and the modulation by catecholamines of aldosterone release were studied in isolated rat adrenal cell suspensions. Isoproterenol, norepinephrine and epinephrine, but not dopamine, caused statistically significant increase in aldosterone release. Both prazosin (alpha 1 antagonist) and yohimbine (alpha 2 antagonist) suppressed the norepinephrine-induced aldosterone release in a dose dependent manner, respectively. Both atenolol (beta 1 antagonist) and ICI 118-551 (beta 2 antagonist) also blocked (-)-isoproterenol-induced aldosterone release in a dose dependent manner, respectively. Neither (-)-isoproterenol nor (+/-)-norepinephrine at concentrations of 10(-6) M potentiated aldosterone release stimulated by angiotensin II or ACTH. These results suggest that catecholamines stimulate aldosteroidogenesis, but it appears unlikely that aldosterone release induced by ACTH or angiotensin-II is modulated by adrenergic stimulation.
Some reports in the literature allow to suspect the existence of an effect of sexual steroids on the adrenal catecholamines. To test this possibility, we have examined the catecholaminergic activity in the adrenal medulla of normal cycling rats in three phases of estrous cycle and of ovariectomized (OVX) rats injected with pharmacological doses of estradiol (ES), 2-hydroxyestradiol (HE) and/or progesterone (P). Adrenomedullary content of norepinephrine (NE) was similar during the estrous cycle, while epinephrine (E) content was increased during diestrous. This increase was concomitant with an increased phenylethanolamine-N-methyltransferase (PNMT) activity. Moreover, the monoamine oxidase (MAO) activity was significantly increased during proestrous, while the catechol-O-methyltransferase (COMT) activity was significantly decreased during estrous. In addition to these observations, ovariectomy caused a significant reduction of the E/NE ratio and of COMT and MAO activities. Administration of ES to OVX rats increased the E content, the E/NE ratio and the COMT activity as compared to vehicle-treated OVX rats. Administration of P to OVX animals led also to a significant increase of the E/NE ratio and of the COMT activity but not of the E content, while the administration of this steroid to OVX rats previously treated with ES only increased the COMT activity. Finally, administration of HE caused non-significant changes in NE and E contents and in MAO, COMT and PNMT activities. We can conclude that sexual steroids seem to be able to modify the catecholamine metabolism in the adrenal medulla and, hence, they could alter the ability of this gland to store and release these amines.
Using light and electron microscopy, we have observed the presence of rays containing medullary tissue extending across the cortex of rat adrenal glands. Within these rays chromaffin cells, as well as collagen and nerve fibers, were present. It is suggested that these endocrine cells may have a paracrine function within the cortex, possibly via their secretory product.
There is increasing evidence that dopamine (DA) inhibits aldosterone production, but the source of DA for this dopaminergic influence is not known. In the present study we examined the adrenal's zona glomerulosa for the presence of DA. Rats maintained on an intake of regular food were killed by decapitation and the adrenal capsule (containing zona glomerulosa) and the remainder of the gland (containing both cortex and medulla) were examined for their content of DA and also for norepinephrine (NE) and epinephrine (E). DA was found in adrenal glomerulosa in substantial quantity, 1.92 +/- 0.17 (SEM) ng/mg wet weight, representing an approximate concentration of DA of 1-100 microM. DA in adrenal capsule represented 12.2% of the total adrenal content of DA. NE and E were also present in glomerulosa, 3.46 +/- 0.32 and 18.7 +/- 2.1 ng/mg respectively, but, unlike DA, about 98% of the total adrenal content of NE and E was contained in adrenal medulla. The NE/E ratio in capsule and medulla were similar, although slightly higher in adrenal medulla, suggesting that the medulla is the source of the NE and E found in glomerulosa. On the other hand, the DA/E ratio was several-fold higher in glomerulosa than medulla--suggesting that glomerulosa DA was derived at least partially from a source other than adrenal medulla. We also found that short-term culturing of the adrenal reduced DA levels to 1/3 that observed in fresh tissue. This could explain in part why cultured glomerulosa has been shown to be more responsive to administered stimuli. In summary, the findings indicate a significant concentration of DA in adrenal glomerulosa, and suggest that the effects of DA on aldosterone production are mediated locally within the adrenal.
The zona glomerulosa of the rat adrenal gland is innervated by catecholaminergic nerves. Using histofluorescence techniques, we observed catecholaminergic plexuses surrounding adrenal capsular and subcapsular blood vessels. Individual varicose nerve fibers that branched off these plexuses were distributed among adrenal glomerulosa cells. This innervation was permanently eliminated after neonatal sympathectomy with guanethidine or 6-hydroxydopamine, but was not affected by ligation of the splanchnic nerve or extirpation of the suprarenal ganglion. At the ultrastructural level, axonal varicosities were commonly observed in close proximity to glomerulosa cells and blood vessels. Nerve fibers and varicosities were found to contain small (30-60 nm) clear vesicles as well as large (60-110 nm) and small (30-60 nm) dense-cored vesicles. In tissue fixed for the dichromate reaction with or without pretreatment with the false transmitter 5-hydroxydopamine, many nerve terminals contained numerous small dense-cored vesicles which are thought to contain catecholamines. These results establish the anatomical substrate for the catecholaminergic innervation of the rat adrenal cortex.
The activity of phenylethanolamine-N-methyl transferase, the enzyme that methylates norepinephrine to form epinephrine, increases
rapidly in the fetal rat adrenal during the day preceding epinephrine accumulation. The developmental increase in enzyme activity
and the accumulation of epinephrine are prevented by fetal hypophysectomy (decapitation). Administration of adrenocorticotrophic
hormone or cortisol acetate largely reverses the effect of fetal decapitation.
Adrenergic regulation of adenylate cyclase activities in the zona glomerulosa (the capsular fraction) and the zona fasciculata-reticularis (the decapsulated fraction) from rat adrenocortical glands has been investigated. Specific binding of [3H]dihydroalprenolol to the membrane from the capsular and the decapsulated fractions was saturable with dissociation constant (Kd) of 4.67 and 5.1 microM, respectively. The receptor density in the capsular and the decapsulated fractions was 230 and 235 fmol/mg protein, respectively. The potencies which isoproterenol, epinephrine, salbutamol, and norepinephrine competed with [3H]dihydroalprenolol binding sites indicted that adrenergic receptors of the capsular and the decapsulated membranes were of the beta 2-type. beta-Adrenergic stimulation of the adenylate cyclase system was observed only in the capsular fraction. This suggests that beta-adrenergic receptors of the capsular membrane are associated with their adenylate cyclase system, but those of the decapsulated membrane are not. Maximum stimulatory concentrations of ACTH and isoproterenol had no additive effect on the capsular adenylate cyclase, indicating that receptors for ACTH and beta-adrenergic agonists are coupled to a common pool of the cyclase.
The application of immunocytochemistry at both light and electron microscopic levels has revealed neuropeptide tyrosine (NPY)-immunoreactive material to be localized to norepinephrine-containing endocrine cells in the adrenal medulla and also to varicose nerve fibers penetrating the adrenal cortex of several mammalian species, including horse, cat, rat, guinea pig and mouse. Correlative electron microscopic immunostaining has revealed that enkephalin and NPY immunoreactivities are co-localized to the same norepinephrine-containing secretory granules. High concentrations of NPY have been extracted from the mouse adrenal gland (1243.7 +/- 122.8 pmol NPY/g wet tissue; mean +/- SE). Chromatographic analysis has shown the extracted material to correspond with pure natural NPY.
In the periphery, dopamine (DA) is a precursor for norepinephrine (NE) and epinephrine (EPI) biosynthesis and is itself a neurotransmitter in sympathetic ganglia. In addition, DA may function as a neurohormone in providing maximum tonic inhibition of aldosterone secretion from the adrenal cortex. We have quantified the catecholamine content of the adrenal gland and have examined factors that regulate DA content of the adrenal cortex. Adult male Sprague-Dawley rats were assigned to one of four groups: adrenal demedullated (ADM); adrenal denervated via splanchnic nerve section (ADN); adrenal demedullated-denervated (DMN); and sham-operated controls (Sham). Ten days after surgery, rats were killed by decapitation, and the adrenals were removed and later assayed for catecholamine content. Compared with Sham, ADM and DMN decreased NE and EPI levels by 92-99% but DA levels by only 57-58%. ADN decreased levels of each catecholamine by 18-26%. These findings indicate that the adrenal cortex contains approximately 40% of the total gland content of DA and less than 8% of the total gland content of NE and EPI. Furthermore, DA in the adrenal cortex does not appear to require an intact splanchnic nerve supply to the adrenal. In a second experiment, we examined the effects of inhibition of catecholamine biosynthesis with alpha-methyl-p-tyrosine (alpha-MPT) on DA content in Sham and ADM rats. In Sham rats, alpha-MPT decreased adrenal DA by 44% and heart NE by 37%. In contrast, treatment of ADM rats with alpha-MPT increased adrenal DA by 49% but decreased heart NE by 36%.(ABSTRACT TRUNCATED AT 250 WORDS)
The intraadrenal distribution of free and sulfoconjugated catecholamines and the activity of the catecholamine sulfoconjugating enzyme phenolsulfotransferase in the bovine adrenal gland are described. In the adrenal cortex all three free catecholamines, epinephrine, norepinephrine, and dopamine, were detected in various concentrations. In the adrenal medulla, the relative proportion of the main adrenal catecholamines, free epinephrine and free norepinephrine, was found to be higher in the medullary sections derived from the subcortical areas where the ratio of epinephrine to norepinephrine was 8:1 than in the centre of the organ where norepinephrine levels reached those of epinephrine. Free dopamine, representing about 1.0% of the total catecholamine content was distributed in the same pattern as epinephrine or the sum of epinephrine and norepinephrine, revealing a significant positive correlation between regional dopamine and epinephrine plus norepinephrine (r = 0.97) as well as between dopamine and epinephrine (r = 0.96). Phenolsulfotransferase activity was present in both medulla and cortex. Dopamine sulfate was detected in relatively small concentration in all cortical and medullary layers, but norepinephrine sulfate and epinephrine sulfate were not present. The meaning of this distribution of individual catecholamines and phenolsulfotransferase activity in both cortex and medulla is discussed.
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