Drinking behaviour in the cat induced by renin, angiotensin I, II and isoprenaline.
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1. Angiotensin I, II and hog renin, infused into the lateral cerebral ventricles (I.C.V.) of water replete cats, each induced water drinking behaviour. 2. Intravenous infusion of high doses of angiotensin I or II also elicited a drinking response. The dipsogenic effect of I.V. renin was not marked. 3. Drinking in response to I.C.V. angiotensin II was abolished after autonomic ganglion blockade with I.V. hexamethonium or pempidine and was significantly reduced after I.V. atropine methonitrate. 4. The dipsogenic response to I.C.V. angiotensin II was unaffected by either peripheral adrenergic neurone blockade with I.V. bethanidine, alpha-adrenoceptor blockade with phentolamine or beta-adrenoceptor blockade with sotalol. 5. Atropine, atropine methonitrate, hexamethonium and pempidine given I.C.V did not inhibit the diposgenic response to I.C.V. angiotensin II. 6. Bethanidine I.C.V. produced a dose related reduction in the dipsogenic response to I.C.V. angiotensin II. 7. The alpha-adrenoceptor blocking agents tolazoline and phenoxybenzamine given I.C.V did not affect angiotensin induced drinking but the response was regularly inhibited by phentolamine I.C.V. 8. The beta-adrenoceptor blocking agents propranolol and practolol given I.C.V. each inhibited angiotensin induced drinking. The L-isomer of propranolol was a more effective blocker than the D-isomer. 9. Isoprenaline given I.C.V induced drinking in ten of sixteen cats. Subcutaneous administration of isoprenaline also elicited drinking but the onset of the response was delayed and the amount consumed slightly less than after I.C.V infusion. (+info)
Gustatory-salivary reflexes induce non-adrenergic, non-cholinergic acinar degranulation in the rat parotid gland.
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In the presence of the muscarinic blocker atropine, the alpha-adrenoceptor blocker phentolamine and the beta-adrenoceptor blocker propranolol (2 mg kg(-1) of each, I.P.), the numerical density of parotid acinar secretory granules was reduced by 32 % in response to ascorbic acid (0.5 M) applied on the tongue every 30 s over 30 min in awake rats. This non-adrenergic, non-cholinergic (NANC) response was entirely dependent on an intact auriculo-temporal nerve supply. The NANC mechanisms were found to be potentially responsible for almost all of the exocytotic response that occurs in the absence of the three autonomic receptor blockers. No sympathetic contribution to the exocytotic response was found and furthermore, studies in parasympathetically denervated glands showed that the sympathetic contribution to the salivary flow was small. Experimental Physiology (2001) 86.4, 475-480. (+info)
Contrasting effects of phentolamine and nitroprusside on neural and cardiovascular variability.
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The relative contributions of a central neural oscillator and of the delay in alpha-adrenergic transmission within the baroreflex loop in the predominance of low-frequency (LF) cardiovascular variability during sympathetic activation in humans are unclear. We measured R-R interval (RR), muscle sympathetic nerve activity (MSNA), blood pressure (BP), and their variability in 10 normal subjects during sympathetic activation achieved by BP lowering with sodium nitroprusside (SNP) and alpha-adrenergic blockade using phentolamine. SNP and phentolamine induced comparable reductions in BP (P > 0.25). Despite tachycardia and sympathetic activation with both SNP and phentolamine, LF variability in RR, MSNA, and BP increased during SNP and decreased during phentolamine (SNP: RR +20 +/- 6%, MSNA +3 +/- 5%, systolic BP +9 +/- 6%, diastolic BP +7 +/- 5%; phentolamine: RR -2 +/- 7%, MSNA -34 +/- 6%, systolic BP -16 +/- 8%, diastolic BP -13 +/- 4%, P < 0.05 except systolic BP, where P = 0.09). Thus LF variability is reduced when sympathetic activation is induced by alpha-adrenergic blockade. This suggests that alpha-adrenergic transmission within the baroreflex loop may contribute importantly to the predominance of LF cardiovascular variability associated with sympathetic excitation in humans. (+info)
Effects of heat exposure on adrenergic modulation of insulin and glucagon secretion in sheep.
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The effects of heat exposure on the adrenergic modulation of pancreatic secretion were investigated. Five ewes fed at maintenance level (ME base) were housed in thermoneutral (TN; 20 degrees C) and hot (30 degrees C) environments. Heat exposure caused an increase in respiration rate and a slightly higher rectal temperature, and decreases in basal insulin and glucose concentrations. Infusions of saline plus epinephrine caused increases in glucagon and glucose concentrations, and no significant change in insulin secretion. Phentolamine (an adrenergic alpha-antagonist) plus epinephrine augmented insulin secretion; however, this insulin secretory response was inhibited by heat exposure. Propranolol (a beta-antagonist) plus epinephrine produced a slight decrease in insulin secretion in the TN environment, whereas no effect was observed during heat exposure. While glucagon secretion through alpha-adrenergic stimulation was not affected by heat exposure, homeostatic signals controlling insulin release seemed to be affected during heat exposure. We thus hypothesised that insulin concentration is decreased in sheep fed at maintenance level in hot environments, and that this response is mediated in part by a modulation of beta-adrenergic function. (+info)
Phentolamine for vasodilator therapy in left ventricular failure complicating acute myocardial infarction. Haemodynamic study.
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In 15 patients with acute myocardial infarction associated with signs of left ventricular dysfunction, phentolamine was infused intravenously in a dose of 10 mg per hour. This therapy induced a substantial reduction in mean right atrial pressure from 10 to 7 mmHg (1.3 to 0.9 kPa) (P) less than 0.001), and in pulmonary capillary wedge pressure from 20 to 13 mmHg (2.7 to 1.7 kPa) (P less than 0.001). The cardiac index increased from 2.5 to 3.0 1/min per m-minus 2 (P less than 0.001) accompanied by a fall in both the systemic and pulmonary vascular resistances (P less than 0.001). On the other hand, the mean stroke work index did not change significantly after phentolamine, because of tar resistance. With the dose used the mean arterial pressure decreased from 112 to 99 mmHg (14.9 to 13.2 kPa) (P less than 0.001). No adverse effects attributable to the drug treatment were noted. Benefits of this treatment are probably related to reduction in the impedance of left ventricular ejection and possibly to its relaxant effect on the venous tone. The drug may also improve subendocardial perfusion by decreasing left diastolic ventricular pressure. This could possibly limit extension of necrosis. Thus vasodilator therapy appears to be of particular interest in left ventricular failure complicating acute myocardial infarction, where inotropic agents may be contraindicated. (+info)
Effects of phentolamine on coronary blood flow in patients with recent myocardial infarction.
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The myocardial clearance of rubidium may be obtained by praecordial counting after intravenous injection of Rb-minus 86 Cl. Eight patients with recent myocardial infarction had this determination performed before and after the infusion of 10 mg phentolamine at a rate of 0.3 mg/minute. The average predrug myocardial clearance of Rb was 89.3 plus or minus 29.9 ml/min per 100 g myocardium. After phentolamine, the average myocardial clearance rose to 117.3 plus or minus 33.3 ml/min per 100 g myocardium (P LESS THAN 0.01). An explanation for this findings is presented as well as its possible clinical applications. (+info)
Inhibitory effects of clonidine and BS 100-141 on responses to sympathetic nerve stimulation in cats and rabbits.
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1. In pithed cats, the spinal sympathetic outflow was stimulated preganglionically at segments C7 and T1 and heart rate responses and nictitating membrane tone were measured in parallel. 2. Clonidine and a related drug, BS 100-141 (N-amidino-2(2,6-dichlorophenyl)acetamide hydrochloride), caused a dose-dependent inhibition of the stimulation-induced tachycardia but did not inhibit responses of the nictitating membrane. The inhibition of heart rate was antagonized by the alpha-adrenoceptor blocking drug, phentolamine. 3. In isolated hearts of rabbits, noradrenaline release in response to adrenergic nerve stimulation was reduced by clonidine and BS 100-141 and the effect was antagonized by phentolamine. 4. The results support the view that presynaptic alpha-adrenoceptors are involved in the regulation of transmitter release from adrenergic nerves. Cardiac adrenergic nerves appear more sensitive to alpha-adrenoceptor-mediated inhibition of inpulse transmission than the sympathetic nerves to the nictitating membrane. (+info)
The responses of the isolated, blood-perfused spleen of the dog to angiotensin, oxytocin and vasopressin.
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1 The responses of the smooth muscle of the capsule and blood vessels of the isolated, blood-perfused spleen of the dog to angiotensin, oxytocin and vasopressin have been investigated and compared to the actions of the catecholamines, adrenaline and noradrenaline.2 Increasing doses of each of the three polypeptides cause graded increases in splenic vascular resistance and reductions in spleen volume.3 Doses of the polypeptides which evoked increases in splenic vascular resistance not significantly different from increases produced by chosen doses of each catecholamine caused significantly smaller reductions in spleen volume.4 The time-course of action of the polypeptides on the splenic vascular smooth muscle is different since the time to 50% recovery from vasopressin is highly significantly longer than that for equieffective doses of either angiotensin or oxytocin.5 Phenoxybenzamine, in a dose which almost blocked the actions of the catecholamines, increased the responses of the vascular and capsular smooth muscle to oxytocin, vasopressin and angiotensin. This increase was not observed with another alpha-adrenoceptor blocking agent, phentolamine.6 The significant species variation in the responses of the smooth muscle of the spleen to polypeptides and catecholamines are discussed and the results are considered in the context of the possible physiological roles of the polypeptides in haemorrhage. (+info)