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ABSTRACT: Cerebral blood flow in either the cortex, thalamic region or the brain stem, as well as somatosensory evoked potentials were measured in a model of moderate cerebral ischaemia in three groups of anaesthetized spontaneously hypertensive rats. The rats were bled to reduce evoked potential amplitudes to approximately 50-60% of pre-haemorrhage control. The consequent blood pressure fall reduced blood flow to approximately 65, 80 and 85% of pre-haemorrhage control in the cortical, thalamic and brain stem regions, respectively, as measured with a laser Doppler flowmeter. Hexamethonium (10 mg kg-1 i.v.), an autonomic ganglion blocker, caused vasodilation and a slight (7-13 units of prebleeding control) increase in blood flow in all the three regions, and the somatosensory evoked potentials normalized. In addition, the latency of the first evoked potential component decreased toward prebleeding values. Heart rate decreased and a transient decrease was also observed in mean arterial pressure despite an attempt to keep it constant with a pressure regulating reservoir. It is possible that the slightly increased regional cerebral blood flow after hexamethonium injection can explain the improved cerebral function as indicated by the enhanced somatosensory evoked potentials. However, the results might also indicate an autonomic regulation of afferent sensory pathways.
Acta Physiologica Scandinavica 10/1996; 158(1):21-8. · 2.55 Impact Factor
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ABSTRACT: Hypertonic solutions act in the central nervous system (CNS) to increase mean arterial blood pressure (MAP) by activation of the sympathoadrenal axis. However, adrenal nerve activity (pre- and postganglionic nerve fibers) has not been determined during central osmotic stimulation. Therefore, these experiments evaluated adrenal (AdSNA) and renal (RSNA) sympathetic nerve activity, MAP, and heart rate (HR) following CNS administration of isotonic, hypertonic, and hypotonic sodium chloride solutions in chloralose-anesthetized rats. Injection of isotonic saline (5 microliters) did not alter MAP, HR, RSNA, or AdSNA. However, injection of hypertonic saline (5 microliters of 0.5 M) into the anteroventral portion of the third cerebral ventricle increased MAP (12 +/- 2 mmHg) and decreased HR (16 +/- 6 bpm). In addition, hypertonic saline significantly decreased RSNA (58 +/- 5% control), whereas AdSNA increased (158 +/- 10% control). Injection of hypotonic (5 microliters of 0.05 M) NaCl produced the opposite responses in RSNA (119 +/- 7% control) and AdSNA (86 +/- 5% control) and had no significant effect on MAP or HR. Furthermore, pre- and postganglionic adrenal nerve fibers responded similarly to changes in CNS osmolality. These results demonstrate that osmotic stimulation produces differential responses in RSNA and AdSNA, but not in pre- and postganglionic adrenal nerve fibers.
Brain Research Bulletin 02/1996; 39(4):205-9. · 2.82 Impact Factor
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ABSTRACT: Recently emerging evidence has indicated that efferent renal sympathetic nerve activity (RSNA) is increased in congestive heart failure (CHF). In the present study the cyclic activity of the renal nerve in the normal and CHF rat was studied. An ischaemic myocardial lesion resulting in CHF was induced by left coronary artery ligation. Sham-operated rats subjected to thoracotomy served as normal controls. Renal sympathetic nerve activity was recorded under chloralose anaesthesia. The neural cycle activity was significantly higher in CHF (47 +/- 3%) compared with sham-operated rats (34 +/- 3%, P < 0.005). Baroreceptor control of RSNA was significantly attenuated in CHF compared with normal control rats (P < 0.005). In response to noxious thermal stimulation by 48 degrees C water immersion of the tail tip, the increase of RSNA was significantly higher in CHF compared with sham-operated rats. A stepwise 15% blood volume expansion over 5 min which induced no alterations of blood pressure or heart rate (HR) resulted in a gradual decrease of RSNA in control rats by approximately 25% at the end of the volume expansion procedure. In CHF rats however, there was no significant change in RSNA during volume expansion. It is concluded that in CHF rats: (1) efferent RSNA is increased; (2) baroreceptor control of RSNA is decreased; (3) RSNA in response to cutaneous thermal noxious stimulation is exaggerated; and (4) RSNA inhibition by cardiopulmonary receptors is blunted.
Acta Physiologica Scandinavica 03/1994; 150(3):259-66. · 2.55 Impact Factor
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ABSTRACT: The aim of this study was to investigate the blood flow in the adrenal cortex of the rat. Relative changes in the adrenal cortical blood flow were continuously measured by Laser Doppler flowmetry in 33 chloralose-anaesthetized artificially ventilated rats during electrical stimulation (1 ms, 5 V) of the left great splanchnic nerve (LGSN), which conveys both pre- and post-ganglionic nerve fibres to the adrenal gland. Laser Doppler flux (LDF) was decreased and regional resistance (RR) was increased by augmenting nerve stimulation at increasingly higher frequencies (2, 4, 8, 20 and 40 Hz). The decrease in LDF, when compared to pre-drug stimulations at 4 Hz was partially or totally inhibited by the adrenergic blocking agents trimethaphan (TRIM), guanethidine (GUA) and alpha 1-blockade with prazosin (PRAZ). Furthermore, both the decrease in LDF and the increase in RR were either completely or partially blocked by stimulation at 40 Hz after TRIM-treatment and GUA-treatment. It is concluded that the adrenal cortex in the rat is innervated by post-ganglionic adrenergic nerve fibres, which are involved in the regulation of blood flow in the adrenal cortex.
Acta Physiologica Scandinavica 10/1993; 149(1):23-30. · 2.55 Impact Factor
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ABSTRACT: The differential effects of the alpha-2 adrenergic agonist, clonidine, on blood pressure, renal sympathetic nerve activity (RSNA) and renal responses were investigated in conscious as well as anesthetized congestive heart failure (CHF) rats and normal control animals. After the stepwise increments of i.v. clonidine infusion (5, 15 and 30 micrograms/hr for 1 hr), mean arterial pressure gradually decreased in CHF, but increased significantly in the control animals at the higher doses. Urinary volume, sodium and potassium excretions were significantly higher in the normal control animals after the clonidine 30-micrograms/hr infusion compared with the CHF rats. There were almost immediate decreases in RSNA in both the CHF and control groups. Although the control animals reduced RSNA to about 5%, the CHF rats retained 36.5% of their respective control values after clonidine administration. Base-line plasma immunoreactive atrial natriuretic peptide were increased 7-fold in the CHF rats compared to controls. After clonidine, immunoreactive atrial natriuretic peptide increased more than 3-fold in the normal rats, whereas no changes were observed in the CHF group. Our data show that clonidine decreases RSNA in CHF and that the natriuretic and that diuretic effects of an alpha-2 receptor agonist are blunted in experimental CHF. Furthermore, the different mean arterial pressure response in the CHF and control groups at higher doses of clonidine may suggest down-regulation of the vascular alpha-2 adrenergic receptor in CHF.
Journal of Pharmacology and Experimental Therapeutics 07/1992; 261(3):1129-35. · 3.83 Impact Factor
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ABSTRACT: The aim of the study was to compare pre-ganglionic adrenal nerve activity (pre-aSNA) to post-ganglionic adrenal nerve activity (post-aSNA) in rats after administration of 2-deoxy-D-glucose (2-DG, 500 mg kg-1, i.v.), which mimicks a central hypoglycaemia or to the response in pre-aSNA and post-aSNA to hypoglycaemia after injection of insulin (5U). Renal postganglionic sympathetic nerve recordings (rSNA) in a separate group was used as a reference. Adrenal or renal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar-rats. Trimethaphan, a short-lasting ganglionic blocker, was administered i.v. (10 mg kg-1) in order to test for pre- or post-aSNA in the adrenal nerves. The adrenal nerves was considered to contain predominantly post or preganglionic fibres, respectively if the nerve activity in the adrenal nerve decreased (post-aSNA) or increased (pre-aSNA). In contrast, all renal nerves showed almost a pure postganglionic activity. Post-aSNA responded with a tendency to increase after the 2-DG injection. The highest value (percentage change from control) 5 min after injection was 12 +/- 9%. The pre-aSNA increased with values of 99 +/- 52% at 3 min and 86 +/- 31% at 5 min (percentage change from control). The activity in the rSNA was only slightly decreased after the injection of 2-DG when compared to pre-drug control activity. There was a significant difference between the pre-aSNA vs. post-aSNA at 1 min (P less than 0.05), 3 min (P less than 0.01) and 5 min (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Acta Physiologica Scandinavica 07/1992; 145(2):169-75. · 2.55 Impact Factor
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ABSTRACT: The aim of the study was to compare pre- (pre-aSNA) and postganglionic adrenal sympathetic nerve activity (post-aSNA) and postganglionic renal sympathetic nerve activity (rSNA) in rats during arterial baroreceptor activation and haemorrhage. Adrenal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar rats. To test for pre-aSNA or post-aSNA in adrenal nerves, a ganglionic blocker, trimethaphan (10 mg kg-1), was administered i.v. If the nerve activity in the adrenal nerve decreased or increased the nerve was considered to contain predominantly post- or preganglionic fibres, respectively. In contrast, the renal nerves exhibit an almost pure postganglionic activity. Baroreceptor activity was tested by activation of baroreceptors, with an alpha-receptor agonist, phenylephrine, which was slowly infused (0.5-2 micrograms kg-1 min-1), and to deactivate the baroreceptors the rats were bled down to 50 mmHg for 8 min. The experiments showed that all tested nerve types were baroreceptor dependent. There were no significant differences between the slopes relating nerve activity inhibition to increase in blood pressure (infusion of phenylephrine). During maximal inhibition there was a difference between the rSNA and pre-aSNA, 87 +/- 4%, n = 6, and 68 +/- 6%, n = 10 (P less than 0.01) of the control value, respectively. The maximal inhibition of post-aSNA was 80 +/- 3%, n = 7, of the control value. During haemorrhage there was a difference between the nerve populations. Pre-aSNA responded with a marked increase within 1.5 min (159 +/- 29% of control, n = 7) and was then maintained at that level until retransfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Acta Physiologica Scandinavica 04/1992; 144(3):317-23. · 2.55 Impact Factor
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Journal of hypertension. Supplement: official journal of the International Society of Hypertension 01/1992; 9(6):S58-9.
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ABSTRACT: The aim of this study was to examine and characterize the post-ganglionic innervation of the adrenal gland, using a neurophysiological nerve recording technique. Adrenal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar rats. To test for post-ganglionic nerve activity, trimethaphan, a ganglionic blocker, was given intravenously. About 60% of the adrenal nerve preparations tested responded with a marked decrease in nerve activity (to 52 +/- 11% of pre-trimethaphan activity, P less than 0.01), while other nerves responded with an increase in activity (to 152 +/- 29% of pre-trimethaphan activity, P less than 0.01). Based on these responses, the nerves were considered to contain predominantly post- or preganglionic fibres respectively, and the difference in response to an intravenous injection of trimethaphan between the two groups was significant (P less than 0.01). It was also demonstrated that the post-ganglionic adrenal nerve activity had a greater variability in firing pattern than preganglionic adrenal nerve activity. We also examined whether there was any cardiac rhythmicity in the investigated nerves. There was a weak cardiac rhythmicity in six out of 12 post-ganglionic adrenal nerves, but there was no cardiac rhythmicity in the remaining six post-ganglionic nerves, and we observed no cardiac rhythmicity in preganglionic nerves. In contrast, renal sympathetic nerves showed a profound cardiac rhythmicity. Our results might explain recent histological findings of a direct post-ganglionic innervation of the adrenal cortex. We speculate that this nerve population is involved in steroid synthesis indirectly via regulation of the cortical blood flow or directly via a direct innervation of parenchymal cells in the adrenal cortex.
Acta Physiologica Scandinavica 01/1991; 140(4):491-9. · 2.55 Impact Factor
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ABSTRACT: In a previous study, prolonged low-frequency muscle stimulation, inducing dynamic contractions in the hind leg of unanaesthetized rats, was shown to give rise to a hypoalgesia. The increase in pain threshold, measured as squeak threshold to noxious electric pulses, lasted 3 h. In the present study, the involvement of the endogenous opioid system in the post-stimulatory analgesia was investigated using selective opioid receptor antagonists. The post-stimulatory analgesia was completely reversed back to prestimulatory control levels by naloxone, 1 mg kg-1. ICI 154,129 and MR 2266 BS, selective delta- and kappa-receptor antagonists respectively, did not significantly influence the post-stimulatory analgesia, although ICI 154,129 had a minor pain threshold-lowering effect. Rats pretreated with beta-funaltrexamine, a mu-receptor antagonist, did not exhibit any post-stimulatory analgesia. These results suggest that opioid systems are involved in the increase in pain threshold after muscle stimulation and that the analgesic response is both elicited and maintained by the mu-receptor.
Acta Physiologica Scandinavica 12/1990; 140(3):353-8. · 2.55 Impact Factor
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ABSTRACT: Irindalone is a new antihypertensive agent with affinity to serotonin (5-HT2) receptors and at higher concentrations also to alpha 1-adrenoceptors. The present study was designed to evaluate the relative importance of the antagonism of central and peripheral alpha 1- and 5-HT2-receptors in the blood pressure lowering properties or irindalone after acute administration. In conscious Sprague-Dawley rats intravenous irindalone (0.05-1.5 mg/kg) dose-dependently reduced the blood pressure. In the same dose-range irindalone antagonized pressor responses to phenylephrine and electrical stimulation of the spinal sympathetic outflow (SNS) in the pithed rats, indicating that the acute blood pressure lowering effect is primarily related to the blockade of alpha 1-adrenoceptors. However, the concomitant 5-HT2-receptor blockade may contribute since irindalone in a dose (0.15 mg/kg) where it had no alpha-adrenoceptor blocking properties enhanced the hypotensive response to selective alpha 1-adrenoceptor blockade by prazosin (1 micrograms/kg). We found no evidence that central mechanisms contributed to the blood pressure lowering effect of irindalone. In anaesthetized rats irindalone (1 mg/kg) did not reduce the directly recorded sympathetic nerve activity. Intracerebroventricular administration of irindalone in conscious rats (10-100 micrograms) had no consistent effects on the blood pressure and did not enhance the hypotensive response to intracerebroventricularly administered prazosin (10 micrograms). Finally, the hypotensive response to irindalone was not influenced by depletion of central serotonin stores (by PCPA). It is concluded that the blood pressure lowering effect of irindalone following acute administration is related primarily to blockade of peripheral alpha-adrenoceptors but that the concomitant blockade of 5-HT2-receptors may contribute.
Pharmacology & Toxicology 10/1990; 67(3):199-204.
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ABSTRACT: In a previous study prolonged low-frequency muscle stimulation in the hind leg of the spontaneously hypertensive rat (SHR) was shown to induce a reduction in blood pressure (about 15 mmHg) that lasted for many hours. We showed in that study that endorphin and serotonin systems were involved. In the present study drugs with selective affinity for the serotonin (5-HT) receptors were used to analyse further the involvement of different serotonin systems. In one group of SHR, a prestimulatory dose of metitepine maleate (a 5-HT1 and 5-HT2 receptor antagonist) completely abolished the post-stimulatory depressor response. The long-lasting depressor response was still present, although less pronounced, after a bolus dose of the 5-HT2 blocking agent ritanserin (R 55667) at the start of stimulation. The 5-HT3 receptor antagonist ICS 205-930 did not influence the response at all, nor did the selective 5-HT1a receptor agonist 8-OH-DPAT enhance the depressor response. These results indicate that the reduction in blood pressure after muscle stimulation is mainly mediated by the 5-HT1 receptor.
Acta Physiologica Scandinavica 07/1990; 139(2):305-10. · 2.55 Impact Factor
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ABSTRACT: The aim of this study was to examine the effect of i.v. morphine on sympathetic nerve activity (SNA) in the rat. Adrenal SNA and renal SNA were recorded simultaneously, together with mean arterial pressure and heart rate, in chloralose-anesthetized, artificially ventilated rats. Separate groups of rats were subjected to vagotomy. In intact rats, i.v. injection of morphine (1 mg/kg) caused an immediate transient depressor response. Within 1-3 sec, renal SNA was markedly inhibited in parallel with hypotension and bradycardia. After a few minutes, mean arterial pressure and renal SNA returned toward base-line levels, and subsequently they declined gradually again below base line. Adrenal SNA, however, showed an immediate brief increase. In the vagotomized rats, an extended renal SNA excitation occurred, accompanied by a rise in mean arterial pressure. After about 15 min, these variables returned toward base-line levels. The adrenal SNA excitation still occurred in the vagotomized rats. The renal depressor and the renal and adrenal pressor responses were all abolished by naloxone pretreatment. It is concluded that i.v. injection of morphine induces a highly differentiated response of SNA. A pronounced immediate increase in adrenal SNA occurs in parallel with renal SNA inhibition. The renal nerve inhibition is mainly reflexly obtained by opioid receptor-mediated activation of vagal afferents. The predominant central action of morphine seems to be sympathetic excitation which is also mediated through opioid receptors.
Journal of Pharmacology and Experimental Therapeutics 06/1990; 253(2):655-60. · 3.83 Impact Factor
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ABSTRACT: Cerebral blood flow (CBF, by laser Doppler flowmetry) and extracellular cortical concentrations (by microdialysis) of adenosine, inosine, xanthine, hypoxanthine, and lactate were measured together with somatosensory evoked potentials (SEP) in chloralose-anaesthetized spontaneously hypertensive rats (SHR) during relative cerebral ischemia induced by hypotensive hemorrhage. Reduction of mean arterial blood pressure (MABP) to 40-50 mm Hg, which decreased SEP to about 50% of prebleeding control level, decreased CBF only to about 75% of control due to cerebrovascular "autoregulation." A secondary, marked rise in cerebrovascular resistance (CVR) occurred after about 15 min in parallel with a striking increase in heart rate (after initial bradycardia). This late rise in heart rate is probably elicited by relative ischemia in medullary centers. The increase in CVR might indicate increased sympathetic nerve activity to the circle of Willis and large cerebral arteries. Cortical lactate increased initially but started to decline after about 30 min, and after 2 h it was not significantly higher than control. Cortical adenosine, inosine, hypoxanthine, and xanthine increased slowly and were significantly elevated after 50 min of hemorrhage. After 80 min, adenosine and inosine had returned to initial levels, while hypoxanthine and xanthine were further elevated. Despite the apparent partial recovery of metabolic disturbances during late hemorrhage, and with a blood flow maintained at 75% of resting control, SEP did not improve. It is suggested that the depression of SEP is not primarily caused by circulatory-metabolic derangements, but instead by activation of specific inhibitory systems.
Journal of Cerebral Blood Flow & Metabolism 07/1989; 9(3):364-72. · 5.01 Impact Factor
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Acta physiologica Scandinavica. Supplementum 02/1988; 571:97-105.
