Autonomic & Autacoid Pharmacology
Autonomic and Autacoid Pharmacology (formerly Journal of Autonomic Pharmacology) is an international journal dealing with the interactions of drugs and related substances with the central and peripheral divisions of the autonomic nervous system and its effector organs and tissues. All aspects of basic experimental pharmacology in intact animals, isolated tissues and biochemical systems of tissue fractions are covered. This includes the effects of drugs acting on the autonomic nervous system and its effector organs in humans. The drugs under examination are primarily those with actions on the cardiovascular, respiratory and gastrointestinal systems of the body. The effector organs of the autonomic nervous system is interpreted in its widest sense to include substances affecting smooth and cardiac muscle in general. The scope of the journal has widened to include the pharmacology of autacoids including angiotensin, endothelin, kinins, prostaglandins, leukotrienes, opioids, cytokines, histamine and 5-hydroxytryptamine.
- WebsiteAutonomic and Autocoid Pharmacology website
Other titlesAutonomic & autacoid pharmacology (Online), Autonomic and autacoid pharmacology
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Publications in this journal
Article: Topical anaesthesia does not affect cutaneous vasomotor or sudomotor responses in human skin.[show abstract] [hide abstract]
ABSTRACT: The effects of local sensory blockade (topical anaesthesia) on eccrine sweat glands and cutaneous circulation are not well understood. This study aimed to determine whether topical lidocaine/prilocaine alters eccrine sweat gland and cutaneous blood vessel responses. Sweating (capacitance hygrometry) was induced via forearm intradermal microdialysis of five acetylcholine (ACh) doses (1 × 10(-4) to 1 × 10(0) m, 10-fold increments) in control and treated forearm sites in six healthy subjects. Nitric oxide-mediated vasodilatory (sodium nitroprusside) and adrenergic vasoconstrictor (noradrenaline) agonists were iontophoresed in lidocaine/prilocaine-treated and control forearm skin in nine healthy subjects during blood flow assessment (laser Doppler flowmetry, expressed as% from baseline cutaneous vascular conductance; CVC; flux/mean arterial pressure). Non-linear regression curve fitting identified no change in the ED50 of ACh-induced sweating after sensory blockade (-1.42 ± 0.23 logM) compared to control (-1.27 ± 0.23 logM; P > .05) or in Emax (0.43 ± 0.08 with, 0.53 ± 0.16 mg cm(-2) min(-1) without lidocaine/prilocaine; P > .05). Sensory blockade did not alter the vasodilator response to sodium nitroprusside (1280 ± 548% change from baseline CVC with, 1204 ± 247% without lidocaine/prilocaine) or vasoconstrictor response to noradrenaline (-14 ± 4% change from baseline CVC with, -22 ± 14% without lidocaine/prilocaine; P > 0.05). Cutaneous sensory blockade does not appear to alter nitric oxide-mediated vasodilation, adrenergic vasoconstriction, or cholinergic eccrine sweating dose-response sensitivity or responsiveness to maximal dose. Thus, lidocaine/prilocaine treatment should not affect sweat gland function or have blood flow implications for subsequent research protocols or clinical procedures.Autonomic & Autacoid Pharmacology 05/2013;
Article: The role of NO in the posterior hypothalamus in amygdala-generated pressor responses in conscious rats.[show abstract] [hide abstract]
ABSTRACT: 1 The nitrergic system modulates cardiovascular functions of the central nucleus of amygdala (CeA) and the posterior hypothalamus (PH) which are involved in the central regulation of the cardiovascular system. The aim of this study was to investigate the contribution of nitric oxide (NO) in the PH in eliciting cardiovascular responses produced through electrical stimulation (ES) of the CeA. Rats were implanted with a stimulation electrode and a parenchymal cannula system into the CeA and a parenchymal cannula or a microdialysis probe into the PH. The next day, the femoral artery was cannulated for haemodynamic measurement. The CeA was electrically stimulated to produce cardiovascular response. The nitric oxide synthetase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 400 nmol/100 nl) or artificial cerebrospinal fluid were injected into the PH or the CeA before the ES of the CeA. The dialysates were collected from the PH to determine the L-citrulline and the L-glutamic acid levels. 2 L-NAME injection into the CeA but not to the PH suppressed the increases in the mean arterial pressure produced by the ES of the CeA significantly; however, heart rate was not affected by L-NAME injection into either the PH or the CeA. L-citrulline and L-glutamic acid levels in the PH were shown to be increased by the ES of the CeA. 3 NO is involved between the PH and the CeA which has a considerable role in the central regulation of the cardiovascular system.Autonomic & Autacoid Pharmacology 03/2013;
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ABSTRACT: 1 As selective serotonin reuptake inhibitors have an inhibitory effect on nicotinic acetylcholine receptors, they may affect the neuromuscular transmission and interact with neuromuscular blockers. This study was designed to observe the effect of fluoxetine on neuromuscular transmission and its interaction with rocuronium using the rat phrenic nerve hemidiaphragm and rabbit head drop methods. 2 Rat phrenic nerve hemidiaphragms were mounted and stimulated using a train of four pulses (TOF). The effect of fluoxetine was studied on both indirectly and directly stimulated basal twitch responses by plotting cumulative dose response curves (DRCs). DRCs of rocuronium were obtained in the absence, and presence of 5 μm and 20 μm fluoxetine to study its interaction. ED5 , ED50 and ED95 values of rocuronium DRCs in absence and presence of fluoxetine were calculated. 3 Fluoxetine significantly inhibited twitch responses in both indirect and directly stimulated preparations. Fluoxetine (20 μm) caused an increase in the potency of rocuronium such that the ED50 and ED95 values of rocuronium DRCs were significantly decreased. Partially inhibited twitch responses by fluoxetine (100 μm) were not reversed by neostigmine (3.3 μm) or 3,4 diaminopyridine (0.25 μm). 4 Rabbits were given fluoxetine 0.25 mg kg-1 and 1 mg kg-1 orally for 15 days, and on 15th day, rocuronium infusion was given, and time for head drop was recorded. The time of head drop was significantly reduced in fluoxetine pretreated as compared to control group. 5 Fluoxetine blocks the neuromuscular transmission and increases the potency of rocuronium-induced neuromuscular block.Autonomic & Autacoid Pharmacology 03/2013;
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ABSTRACT: 1 This study was conducted to determine whether the atypical opioid analgesic tramadol inhibits the contractility of isolated non-pregnant human myometrium. Ten strips of non-pregnant human myometrium stimulated with 55 mm potassium chloride (KCl) were treated with three concentrations (30, 100 and 300 μm) of tramadol to test for any inhibitory effect of tramadol. The effects of concurrent administration of the ß adrenoceptor antagonist propranolol (1 μm), the guanylyl cyclase and nitric oxide synthase inhibitor methylene blue (20 μm) and the opioid receptor antagonist naloxone (100 μm) with tramadol were also studied. 2 Tramadol caused a concentration-dependent inhibition of KCl-induced myometrial contractility, which was statistically significant at all three concentrations of tramadol used. Propranolol significantly reversed the inhibitory effect of 100 μm tramadol on KCl-induced myometrial contractility but not that of 300 μm tramadol. Neither methylene blue nor naloxone reversed the inhibitory effect of tramadol on KCl-induced myometrial contractility. 3 These results suggest that tramadol inhibits KCl-induced contractility of isolated human myometrium. They also suggest that tramadol relaxes the myometrium due to stimulation of ß(1) adrenoceptors. However, the concentrations of tramadol required to relax the myometrium were high and likely to be attained at toxic doses, rather than therapeutic doses, of tramadol.Autonomic & Autacoid Pharmacology 02/2013;
Article: Non-adrenergic, non-cholinergic, non-purinergic contractions of the urothelium/lamina propria of the pig bladder.[show abstract] [hide abstract]
ABSTRACT: Acetylcholine, and to a lesser extent ATP, mediates neurogenic contractions of bladder smooth muscle. Recently, the urothelium and lamina propria have also been shown to have contractile properties, but the neurotransmitters involved in mediating responses to nerve stimulation have not been investigated. Isolated strips of porcine urothelium with lamina propria were electrically field stimulated and contractions recorded. Drugs interfering with neurotransmission were then employed to identify which neurotransmitters mediated responses. Strips of urothelium/lamina propria developed spontaneous contractions with a frequency of 3.5 ± 0.1 cycles min(-1) and amplitude of 0.84 ± 0.06 g. Electrical field stimulation at 5, 10, and 20 Hz resulted in frequency-related contractions (1.13 ± 0.36 g, 1.59 ± 0.46 g and 2.20 ± 0.53 g, respectively, n = 13), and these were reduced in the presence of tetrodotoxin (1 μm) by 77 ± 20% at 5 Hz, 79 ± 7% at 10 Hz and 74 ± 12% at 20 Hz (all P < 0.01), indicating they were predominantly neurogenic in nature. Neither the muscarinic antagonist atropine (10 μm), the adrenergic neurone blocker guanethidine (10 μm) nor desensitization of the purinergic receptors with α,β-methylene ATP (10 μm) affected the contractile amplitude. Similarly, responses were not affected by the nitric oxide synthase inhibitor l-NNA (100 μm) or drugs that interfere with peptide neurotransmission (capsaicin, NK2 antagonist GR159897, protease inhibitors). In conclusion, electrical depolarization of the nerves present in the porcine urothelium/lamina propria results in frequency-dependent contractions, which are predominantly neurogenic in nature. These contractions are resistant to drugs that inhibit the adrenergic, cholinergic and purinergic systems. The neurotransmitter involved in the responses of this tissue is therefore unknown but does not appear to be a peptide.Autonomic & Autacoid Pharmacology 10/2012; 32(3 Pt 4):53-9.
Article: Enhanced nerve-stimulated muscarinic and neurokinin contractions of ileum from streptozotocin guinea-pigs.[show abstract] [hide abstract]
ABSTRACT: Diabetes mellitus can lead to neuropathy of enteric neurons, resulting in abnormal gut motility. These studies investigated voltage-dependent contributions of muscarinic M(3) receptor activation by acetylcholine and neurokinin NK(1) receptor activation by neurokinins to nerve-stimulated contractions of longitudinal ileal strips from STZ guinea-pigs, a type 1 diabetic model with insulin deficiency, but mild hyperglycaemia. Contractions to bethanechol, substance P methyl ester, and nerve stimulation were greater in diabetic as compared to control ileum. The muscarinic M(3) receptor antagonist 4-DAMP at lower voltages and the neurokinin NK(1) receptor antagonist SR140333 at higher voltages, but not the neurokinin NK(1) receptor antagonist CP-96,345, were more effective at inhibiting nerve-stimulated immediate peak contractions and total areas of contraction of ileum from diabetic as compared to control animals. For diabetic ileum, voltage-dependent increases in the areas of nerve-stimulated contraction were observed in the presence of 4-DAMP and CP-96,345 but not SR140333. At low voltages only, nerve-stimulated release of acetylcholine was greater from diabetic as compared to control ileum. Fluorescence intensity of tachykinin-like immunoreactivity was increased in ileal myenteric ganglia from diabetic as compared to control animals. In diabetic guinea-pigs, stronger ileal nerve-stimulated contractions reflected increased release of acetylcholine at lower voltages and tachykinins at higher voltages, as well as increased sensitivity of smooth muscle M(3) and NK(1) receptors to acetylcholine and tachykinins. Hypoinsulinaemia may be a primary contributor to intestinal motility dysfunction in type 1 diabetes mellitus.Autonomic & Autacoid Pharmacology 06/2012; 32(3 Pt 4):23-39.
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ABSTRACT: The atypical opioid analgesic tramadol has been shown to provide beneficial clinical and urodynamic effects in patients with detrusor overactivity. The effect of tramadol on isolated detrusor muscle has not been studied. This study investigated the ability of tramadol to inhibit acetylcholine (ACh)-induced contractility of the isolated caprine (goat) detrusor muscle. The effect of three concentrations (30, 100 and 300 μm) of tramadol on 10 caprine detrusor strips contracted by the addition of 100, 200 or 400 μm ACh was studied. The sensitivity of tramadol-induced inhibition of ACh responses to treatment with the β-adrenoceptor antagonist propranolol (1 μm) and the opioid receptor antagonist naloxone (100 μμ) was also studied. Tramadol caused a concentration-dependent inhibition of ACh-induced detrusor contraction that was reversed by raising the concentration of ACh. Propranolol, but not naloxone, reversed the tramadol-induced inhibition of contractions to ACh in the detrusor. These results suggest that tramadol inhibits ACh-induced contractility of the isolated detrusor. They also suggest that tramadol does so by an indirect anticholinergic mechanism involving the stimulation of β-adrenoceptors. Tramadol may be useful in managing clinical conditions requiring relaxation of the detrusor muscle. Although the concentrations of tramadol needed to relax the detrusor were relatively high, these could be clinically attained via intravesical administration.Autonomic & Autacoid Pharmacology 02/2012; 32(1 Pt 2):15-22.
Article: Metformin reduces vascular production of vasoconstrictor prostanoids in fructose overloaded rats.[show abstract] [hide abstract]
ABSTRACT: Metformin is a hypoglycaemic drug currently used to increase insulin sensitivity in the treatment of type 2 diabetes and metabolic syndrome. Its main mechanism of action is through activation of AMP-activated protein kinase, an enzyme that regulates cellular and whole organ metabolism. The fructose-overloaded rat is an experimental model with features that resemble human metabolic syndrome. We have previously reported alterations in vascular prostanoids (PR) in this model. The aim of this study was to analyse the effects of metformin treatment on blood pressure, metabolic parameters and PR production in aorta and mesenteric vascular bed (MVB) from fructose-overloaded animals. Four groups of male Sprague-Dawley rats were used: control, fructose overloaded (10% w/v fructose), metformin treated (50 mg kg(-1) day(-1) ) and fructose-overloaded treated with metformin. Rats with fructose overload had significantly elevated systolic blood pressure, glycaemia, triglyceridaemia, cholesterolaemia and insulinaemia compared with controls. Except for insulinaemia, metformin limited all these increases in fructose-overloaded animals. Fructose overload reduced prostacyclin levels in aorta and MVB, but prostaglandin E(2) levels were only reduced in MVB. Metformin treatment reduced the levels of the vasoconstrictor prostaglandins, PGF(2) α and thromboxane, in both vascular preparations from fructose-overloaded rats. PGF(2) α levels were significantly reduced by metformin in controls. In conclusion, one of the mechanisms by which metformin reduced blood pressure in this model is by decreasing vasoconstrictor prostaglandin production.Autonomic & Autacoid Pharmacology 02/2012; 32(1 Pt 2):9-14.
Article: Protective effects of a magnesium magnetic isotope (Mg(25) )-exchanging nanoparticle ((25) MgPMC(16) ) on mitochondrial functional disorders in esmolol-induced cardiac arrest in rats.[show abstract] [hide abstract]
ABSTRACT: In cardiac surgery, agents are needed to produce temporary cardiac arrest (cardioplegia). One of these agents is esmolol (ESM) which is a short-acting selective beta-1 adrenergic receptor antagonist and its overdose causes diastolic ventricular arrest. The (25) MgPMC(16) (porphyrin adducts of cyclohexil fullerene-C60) is known as a nanoparticle which has a cardioprotective effect when the heart is subjected to stressful conditions. In this study, we aimed to confirm the deleterious effects of ESM overdose on cardiac mitochondria and identify any protective effects of (25) MgPMC(16) in male Wistar rats. Esmolol 100 mg kg(-1) (LD50 = 71 mg kg(-1) ) was injected intravenously (i.v.) into tail vein to induce cardiac arrest. This dose was obtained from an ESM dose-response curve which induces at least 80% arrest in rats. (25) MgPMC(16) at three different doses (45, 90 and 224 mg kg(-1) ) was injected i.v. as pretreatment, eight hours before ESM injection. (25) MgCl(2) or (24) MgPMC(16) were used as controls. Following cardiac arrest, the heart was removed and the mitochondria extracted. Mitochondrial viability and the adenosine 5'-diphosphate sodium salt hydrate/Adenosine 5'-triphosphate disodium salt hydrate (ADP/ATP) ratio were measured as biomarkers of mitochondrial function. Results indicate that (25) MgPMC(16) caused a significant increase in mitochondrial viability and decrease in ADP/ATP ratio. No significant changes were seen with (24) MgPMC(16) or (25) MgCl(2) . It is concluded that cardiac arrest induced by ESM overdose leads to a significant decrease in mitochondrial viability and their ATP levels, whereas pretreatment by (25) MgPMC(16) can protect mitochondria by increasing ATP level through liberation of Mg into cells and the improvement of hypoxia.Autonomic & Autacoid Pharmacology 08/2011; 32(1 Pt 2):1-7.
Article: Effect of IL-1β and TNF-α vs IL-13 on bronchial hyperresponsiveness, β2-adrenergic responses and cellularity of bronchial alveolar lavage fluid.[show abstract] [hide abstract]
ABSTRACT: 1 Levels of IL-13, IL-1β and TNF-α are increased in bronchial lavage fluid of asthmatics and induce certain significant features of bronchial asthma including airway hyper-responsiveness (AHR). In this study, we have investigated the effect of these cytokines in naïve mice and those sensitized to ovalbumin (OVA) on bronchoconstrictions to methacholine (MCh) and the functional antagonism induced by β2 -adrenoceptor agonism. 2 Naïve or OVA-sensitized mice were treated for 3 days with IL-1β (250 U), TNF-α (150 ng), IL-13 (5 μg) or combinations of IL-1β with TNF-α or IL-1β with IL-13. MCh-induced bronchoconstriction and its sensitivity to albuterol, a β2-adrenoceptor agonist, was assessed 24 h after the last cytokine administration. 3 In naïve mice, responsiveness to MCh was significantly increased by the combination of IL-1β and TNF-α, IL-13 alone or in combination with IL-1β, but not by treatment with IL-1β or TNF-α alone. Similar results were obtained in OVA-sensitized mice except that treatment with IL-13 alone did not increase sensitivity to MCh. 4 In naïve mice, albuterol sensitivity was only significantly attenuated by treatment with IL-1β and TNF-α in combination. In mice sensitized to OVA, albuterol sensitivity was significantly attenuated by treatment with TNF-α, IL-13 or IL-13 in combination with IL-1β. 5 Inflammatory cell influx was increased by all cytokines and combinations except IL-13 in OVA-sensitized mice. 6 Our data do not support a link between inflammatory cell influx and AHR. In addition, the mechanism of IL-13-induced AHR might involve decreased β2-adrenoceptor responsiveness.Autonomic & Autacoid Pharmacology 07/2011; 31(3-4):37-49.
Article: The effect of boric acid on acethylcholine, bethanechol and potasssium-evoked responses on ileum of rat.[show abstract] [hide abstract]
ABSTRACT: 1 The aim of this study was to clarify the effect of boric acid on contractions of rat isolated ileum. 2 Contractile responses expressed as Emax and pD2 for acetylcholine (10(-3)-10(-8) m, Ach), bethanechol (10(-3)-10(-8) m) and potassium (10-80 × 10(-3) m, KCl) were determined in the absence and presence of boric acid (10(-3); 5 × 10(-4); 10(-4) m). 3 The contractile response to Ach in the presence of verapamil (10(-6) or 10(-8) m) or in calcium-free Tyrode's solution was also determined in the absence and presence of boric acid. 4 Boric acid did not affect the contractile response to Ach, bethanechol or KCl. Single or cumulative treatment of boric acid did not affect ileum muscle contraction evoked by KCl. The atropine-resistant component of Ach-induced contraction and 4-diphenyl-acetoxy-N-methyl-piperidine methiodide-resistant component of bethanechol-induced contraction were not inhibited by boric acid (10(-3) m). The contractile response to Ach was reduced in calcium-free Tyrode's solution, and the contractile response was not affected by (10(-8) m). The addition of boric acid (10(-3) m) in combination with verapamil (10(-8) m) did not significantly affect the contractile response to Ach. 5 In conclusion, boric acid does not affect contractions induced by Ach, bethanechol or potassium in rat isolated ileum.Autonomic & Autacoid Pharmacology 07/2011; 31(3-4):50-6.
Article: Angiotensin II modifies the expression of α(1)-adrenoceptors in aorta smooth muscle cells of α(1D)-adrenoceptor knockout mice.[show abstract] [hide abstract]
ABSTRACT: 1 The effect of angiotensin II (Ang II) on α(1A)-, α(1B)-, and a(1D)-adrenoceptors (α(1)-AR) expression was analyzed in aorta smooth muscle cells obtained from wild-type (WT) and knock out of α(1D)-AR (α(1D)-AR KO) mice. 2 The relative abundance of mRNA for the three α(1)-ARs was determined in WT and α(1D)-AR KO aortic smooth muscle cells. There were no significant differences between WT and α(1D)-AR KO cells. 3 As early as 1 h Ang II increased α(1B)-AR mRNA in WT cells ≈ 2 fold compared with control; in contrast, in α(1D)-AR KO cells the α(1B)-AR transcript was ≈ 50% of control. 4 Western blot assays showed that Ang II incremented protein content for α(1A)-AR, 86% and 107% in WT and α(1D)-AR KO cells, respectively. 5 Protein for α(1B)- and α(1D)-ARs did not change significantly with Ang II in both WT and a(1D)-AR KO cells. 6 The effect of Ang II on α(1B)-AR mRNA seems to be influenced by the absence of α(1D)-AR in aortic smooth muscle cells, which might be important to understand the interactions among α(1)-ARs.Autonomic & Autacoid Pharmacology 07/2011; 31(3-4):57-63.
Article: α(1D)-Adrenoceptor regulates the vasopressor action of α(1A)-adrenoceptor in mesenteric vascular bed of α(1D)-adrenoceptor knockout mice.[show abstract] [hide abstract]
ABSTRACT: 1 The pressor action of the α(1A)-adrenoceptor (α(1A)-AR) agonist A61603 (N-[5-(4,5-dihydro-1H-imidazol-2-yl)-2-hydroxy-5,6,7,8-tetrahydronaphthalen-1-yl] methanesulfonamide) and the α(1)-ARs agonist phenylephrine and their blockade by selective α(1)-ARs antagonists in the isolated mesenteric vascular bed of wild-type (WT) mice and α(1D)-AR knockout (KO α(1D)-AR) mice were evaluated. 2 The apparent potency of A61603 to increase the perfusion pressure in the mesenteric vascular bed of WT and KO α(1D)-AR mice is 86 and 138 times the affinity of phenylephrine, respectively. 3 A61603 also enhanced the perfusion pressure by ≈1.7 fold in the mesenteric vascular bed of WT mice compared with KO α(1D)-AR mice. 4 Because of its high affinity, low concentrations of the α(1A)-AR selective antagonist RS100329 (5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy) phenyl]-1-piperazinyl] propyl]-2,4-(1H)-pyrimidinedione) shifted the agonist concentration-response curves to the right in the mesenteric vascular bed of WT and KO α(1D)-AR mice. 5 The α(1D)-AR selective antagonist BMY7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5] decane-7,9-dione) did not modify the A61603 or the phenylephrine-induced pressor effect. 6 The α(1B/D)-ARs alkylating antagonist chloroethylclonidine (CEC) shifted the agonist concentration-response curves to the right and decreased the maximum phenylephrine-induced vascular contraction in KO α(1D)-AR mice when compared to WT mice; however, CEC only slightly modified the contraction induced by A61603. 7 The results indicate that the isolated mesenteric vascular bed of WT and KO α(1D)-AR mice expresses α(1A)-AR, that the pressor action of α(1A)-AR is up-regulated for α(1D)-AR in WT mice and suggest an important role of α(1B)-AR in the vascular pressure evoked by phenylephrine in KO α(1D)-AR mice.Autonomic & Autacoid Pharmacology 07/2011; 31(3-4):64-71.
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ABSTRACT: 1 The effect of pantoprazole on vecuronium-induced neuromuscular blockade in in vivo has not been clearly defined. In this study, we demonstrate that chronic administration, but not acute administration, of pantoprazole alters the pattern of vecuronium-induced neuromuscular blockade. 2 This study was designed to evaluate the effect of acute and chronic administration of pantoprazole on vecuronium-induced neuromuscular blockade using the rat in vivo sciatic nerve-stimulated gastrocnemius preparation. 3 Vecuronium was administered as a slow intravenous infusion (29.41 μg kg(-1) min(-1)) until the gastrocnemius twitch response to sciatic nerve stimulation was completely abolished. The effect of acute (single dose, i.v.) and chronic administration (per oral for 21 days) of pantoprazole (3.64 mg kg(-1)) on vecuronium-induced blockade was assessed by comparing ED50 values, time required for 50% block, ED95 values, block duration and percentage of recovery with respect to control. 4 Acute administration of pantoprazole had no significant effect on any parameter of vecuronium-induced neuromuscular blockade. Chronic administration of pantoprazole significantly reduced vecuronium ED50 value, time for 50% block, ED95 value and percentage recovery from blockade compared with the control group (P<0.05). Reduction in the duration of vecuronium-induced blockade was not significantly affected by chronic treatment with pantoprazole compared with control. 5 On chronic administration, pantoprazole may produce earlier block, quick relaxation and reduces the recovery of vecuronium without affecting its duration of action.Autonomic & Autacoid Pharmacology 02/2011; 31(1-2):31-5.
Article: The effect of losartan and carvedilol on vasopressor responses to adrenergic agonists and angiotensin II in the systemic circulation of Sprague Dawley rats.[show abstract] [hide abstract]
ABSTRACT: 1 Interaction between renin-angiotensin (RAS) and sympathetic nervous systems (SNS) was investigated by examining the effect of cumulative blockade of angiotensin II (Ang II) and adrenergic receptors in normal Sprague Dawley rats. 2 Rats were treated with losartan (10 mg/kg), carvedilol (5 mg/kg), or losartan plus carvedilol (10+5 mg/kg) orally for 7 days. On day 8, the animals were anaesthetized with pentobarbitone and prepared for systemic haemodynamic study. Dose-response relationships for the elevation of mean arterial pressure or change in heart rate (HR) in response to intravenous injections of noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II were determined. 3 Losartan or the combination of losartan with carvedilol blunted vasopressor responses to ME and Ang II. Dose-response relationships for agonist action on HR were significantly inhibited by all treatments except for the combination of losartan and carvedilol on the decrease in HR induced by PE. Carvedilol decreased vasopressor responses to NA, PE and Ang II, and HR responses to NA, ME and Ang II. Combination treatment produced similar effects to losartan on the vasopressor and HR responses but had a greater effect on vasopressor responses to ME and Ang II, and on HR responses to NA and Ang II than carvedilol alone. 4 It is concluded that peripheral vasoconstriction induced by Ang II is partly mediated by adrenergic action and that the vasopressor responses to adrenergic agonists depend on an intact RAS. These observations suggest an interactive relationship between RAS and SNS in determining systemic haemodynamic responses in 'normal' rats.Autonomic & Autacoid Pharmacology 12/2010; 31(1-2):13-20.
Article: Characterization of β-adrenoceptor-mediated relaxation signals in isolated pulmonary artery of Dahl salt-sensitive hypertensive and normotensive rats.[show abstract] [hide abstract]
ABSTRACT: 1 Relaxant responses to isoprenaline (ISO) were studied in the pulmonary arteries of normotensive and hypertensive Dahl salt-sensitive rats. Rats were fed either a high-salt (4.0%) or low-salt (0.14%) diet for 5 weeks. Animals fed a high-salt diet (167/123±2/2 mmHg) had a significantly higher blood pressure compared to those fed a low-salt diet (127/87 ± 2/2 mmHg). 2 Isoprenaline-elicited relaxations were not significantly different in tissues from hypertensive compared to normotensive animals. Responses to ISO were significantly attenuated in denuded tissues and substantially more so in hypertensive compared to normotensive animals. While relaxant responses to ISO were resistant to inhibition by Nω-nitro-L-arginine methyl ester, indomethacin, glibenclamide or a combination of barium chloride and ouabain, they were inhibited by Rp-cAMP, anandamide and acidic buffer. The inhibitory impact of anandamide and acidic buffer was significantly greater in tissues from hypertensive vs. normotensive rats. 3 The resting membrane potential (Em) of smooth muscle cells was -67.0±0.7 mV (n=43 cells) and -66.6±0.8 mV (n=55 cells) in pulmonary arteries from hypertensive and normotensive rats, respectively. Isoprenaline produced hyperpolarization of E(m) which was significant in the blood vessels of hypertensive (-71.6±0.8 mV; n=29 cells) but not normotensive (-68.1±0.7 mV; n=49 cells) rats. 4 The endothelium plays a critical role in β-adrenoceptor-mediated relaxation but nitric oxide is not the mediator for the response. It is possible that the greater hyperpolarization caused by ISO in blood vessels from hypertensive compared to normotensive rats is mediated by activation of TASK-1 channels.Autonomic & Autacoid Pharmacology 10/2010; 31(1-2):1-12.
Article: Extraendothelial and constitutive COX-2 expression is involved in the contractile effect of angiotensin II in the rat aorta.[show abstract] [hide abstract]
ABSTRACT: 1 The role of the extraendothelial and constitutive isoforms of cyclo-oxygenase-2 (COX-2) in the contractile effect of angiotensin II (Ang II) was investigated using thoracic and abdominal aortic rings without endothelium from young Wistar rats. 2 Ang II elicited similar contractions in both aortic segments, and the effect was inhibited by pretreatment with NS398 (a selective COX-2 inhibitor) but not SC-560 [selective cyclo-oxygenase-1 (COX-1) inhibitor]. 3 COX-2 mRNA was expressed under basal conditions in both aortic segments. Additionally, Ang II increased COX-2 mRNA expression in the abdominal but not the thoracic segment, while cycloheximide (a protein synthesis inhibitor) did not affect the contractile response to Ang II in either of the two segments; this suggests that the effect is not associated with de novo COX-2 synthesis. 4 In conclusion, the basal amount of COX-2 found in aortic smooth muscle cells is sufficient to explain the production of the prostanoids related to the contractile effect of Ang II. The production of these prostanoids, which are derived from constitutive COX-2, occurs independently of the endothelium vascular system.Autonomic & Autacoid Pharmacology 10/2010; 30(4):205-11.
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