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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of a dopamine D1 receptor antagonist, SCH 23390, were investigated on plasma level of vasopressin after stressful stimuli in rats. The antagonist markedly attenuated the increase in plasma level of vasopressin after electric footshocks but not after s.c. injected hypertonic saline. The antagonist, however, did not significantly change the suppressive vasopressin response to fear-related emotional stress, though the drug suppressed motor behavior of the rat during testing period. These data suggest that dopamine D1 receptors play an important role selectively in the facilitatory vasopressin response to noxious stimuli in rats.
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PMID:A dopamine D1 receptor antagonist, SCH 23390, selectively blocks vasopressin release after noxious stimuli in the rat. 138 18

The aim of this study was to evaluate periventricular dopaminergic and alpha-adrenergic receptor functions in vasopressin (AVP) secretion elicited by central applications of prostaglandin D2 (PGD2) in conscious rats. Intracerebroventricular (i.c.v.) injections of PGD2 (70.9 nmol (25.0 micrograms] produced transient rises in plasma AVP 5 min later, without increasing plasma osmolality, sodium and hematocrit. Arterial pressure and heart rate before and after the PGD2 administrations were not significantly different from those of control rats receiving its vehicle. The PGD2-induced AVP response was not significantly altered by the prior i.c.v. administrations (0.15 mumol) of dopamine receptor antagonists, SCH 23390 or sulpiride, and an alpha-adrenoreceptor antagonist, phenoxybenzamine, performed 10 min before the injections of PGD2. The pretreatments with these catecholamine antagonists were confirmed to significantly prevent the augmentations in plasma AVP 5 min after the i.c.v. applications of 0.75 mumol dopamine or phenylephrine that were considerably larger than the PGD 2-induced AVP response. From these results, we concluded that dopaminergic and alpha-adrenergic receptors in the periventricular regions may not be involved in the AVP secretion stimulated by PGD2.
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PMID:Separation of periventricular dopaminergic and alpha-adrenergic systems from the vasopressin-secreting mechanisms activated by prostaglandin D2. 166 82

The present experiments were designed to test whether the previously reported excitatory and inhibitory effects of dopamine (DA) on the secretion of oxytocin (OT) in lactating rats are exerted at different DA receptor subtypes, and to examine whether one or both of these effects might occur at the level of the posterior pituitary. The basal release of OT in nonsuckled, lactating rats was increased after intravenous administration of the D-1 DA agonist SKF 38393, and this effect, as well as the suckling-induced release of OT, was prevented by treatment with the D-1 DA antagonist SCH 23390, suggesting that DA may exert an important stimulatory influence over OT secretion through an action at the D-1 DA receptor subtype. A small stimulation of basal PRL release was also produced by SKF 38393, but blockade of the D-1 DA receptor did not prevent the suckling-induced release of this hormone. Stimulation of the D-2 DA receptor with PPHT had no effect on basal OT release in nonsuckled rats, but this agent, as well as another D-2 DA agonist, bromocriptine, prevented the suckling-induced release of both OT and PRL. The inhibitory effect of D-2 DA receptor stimulation was blocked by the D-2 DA antagonist domperidone, which increased the basal release of both hormones when given alone. These observations confirm previous findings that inhibitory effects of DA on suckling-induced OT release are mediated through activation of the D-2 DA receptor. To test whether either dopaminergic effect occurs at the level of neurosecretory endings in the neurointermediate lobe (NIL), the stalk-NIL was isolated from lactating rats and perifused in vitro. The stalk-NIL junction was electrically stimulated for 4 s, and the effects of selective D-1 DA and D-2 DA agonists and antagonists on the basal and electrically evoked release of OT and vasopressin (VP) was assessed using the two stimulation (S2/S1) paradigm. Electrical stimulation produced marked increases in release of both neural lobe peptides in a Ca(2+)-dependent manner, and the electrically evoked release of OT, but not VP, was enhanced by the opiate antagonist naltrexone (10 microM). Consistent with the in vivo results, SKF-38393 (20 microM) produced a small, but statistically significant, increase in electrically induced OT release, while SCH 23390 (20 microM) was without significant effect. Neither drug affected the basal release of OT or the basal or electrically stimulated release of VP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Excitatory and inhibitory dopaminergic regulation of oxytocin secretion in the lactating rat: evidence for respective mediation by D-1 and D-2 dopamine receptor subtypes. 183 Dec 47

The aim of this study was to examine in conscious rats the role of periventricular dopamine receptors in vasopressin secretion caused by hypertonicity of the systemic blood. Intracerebroventricular injections of dopamine (0.15 or 0.75 mumol) produced dose-related increases in plasma AVP 90 sec or 5 min later, without affecting plasma osmolality, concentrations of electrolytes, hematocrit, arterial pressure or heart rate. The AVP response to 0.75 mumol dopamine was blocked by its antagonists, SCH 23390, sulpiride and haloperidol, given intracerebroventricularly at a dose of 0.15 mumol 10 or 40 min before the injection of dopamine. The ip injections (2 ml/100 g) of 600 mmol/l NaCl produced, 15 or 30 min later, augmentations in plasma AVP accompanied by elevations in plasma osmolality, sodium and chloride. At a dose of 0.15 mumol given intracerebroventricularly 10 min before the injection of 600 mmol/l NaCl, SCH 23390 or sulpiride inhibited the AVP response at 15 min, and sulpiride or haloperidol inhibited that at 30 min. The increases in plasma osmolality and the electrolytes owing to hypertonic saline were not reduced by these dopamine antagonists. The intracerebroventricular applications of the antagonists followed by those of vehicles for dopamine or by ip injections of 150 mmol/l NaCl were without any effect on plasma AVP or the other plasma variables. On the basis of these results, we concluded that dopamine receptors in the periventricular regions may contribute to AVP secretion in response to hypertonicity of the systemic blood.
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PMID:Participation of periventricular dopamine receptors in vasopressin secretion elicited by hypertonicity of systemic blood in rats. 203 43

The pattern of excessive grooming displayed by rats treated with vasopressin and oxytocin was investigated by calculating the frequencies and contribution of the behavioural elements head washing, body grooming, anogenital grooming, paw licking and scratching. In addition, the suppressive effect on peptide-induced grooming of the dopamine D1 receptor antagonist SCH 23390, of neurotensin and of the opiate receptor antagonists naloxone and naloxone-methobromide was studied. The pattern of excessive grooming induced by vasopressin and by oxytocin was characterized by the contribution of most behavioural elements to the total grooming scores. Oxytocin-induced excessive grooming was characterized by a marked increase in the frequency of anogenital grooming. SCH 23390, neurotensin and naloxone, but not naloxone-methobromide, suppressed excessive grooming induced by vasopressin and oxytocin. It is suggested that dopamine D1 receptors as well as opiate receptors located within the blood-brain barrier are involved in the excessive grooming induced by neurhypophyseal hormones.
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PMID:Neurohypophyseal hormones and excessive grooming behaviour. 227 47

In pentobarbital-anesthetized rats prepared for hemodynamic measurements with Doppler flow probes, intravenous (i.v.) infusions of fenoldopam (2.5 - 160.0 micrograms/kg/min during 15 min) decreased mean carotid artery blood pressure, total peripheral, hindquarter, renal, and mesenteric vascular resistances and increased renal blood flow strongly. The hypotensive effects attained a maximum within the first 3 min of infusion but waned by greater than 30% at the end of fenoldopam administration. This tolerance was observed for calculated total peripheral and hindquarter vascular resistances and to a lesser extent for mesenteric resistance. However, it was absent on the renal vascular bed. Pretreatment with either enalapril, pepstatine, or bilateral nephrectomy significantly increased the hypotensive response to fenoldopam and attenuated the development of tolerance. In conscious spontaneously hypertensive rats (SHR), enalapril potentiated strongly the small blood pressure-lowering activity of fenoldopam. The fall in blood pressure produced by fenoldopam was specifically blocked by SCH 23390, an antagonist of DA-1 dopamine receptors. In normotensive vasopressin-supported pithed rats given phenoxybenzamine plus propranolol, fenoldopam, like SCH 23390, blocked the vasodepressor effects of i.v. bolus injection of dopamine and fenoldopam. In pithed rats, fenoldopam evoked a pressor response that was significantly reduced by enalapril, SCH 23390, or bilateral nephrectomy. In conclusion, fenoldopam exerts DA-1 agonist and antagonist effects. The latter property, together with the activation of the renin-angiotensin system, appears to be responsible for the development of tolerance to the fenoldopam evoked-hypotension. The lack of a tolerance at the level of the renal vascular bed is possibly due to the existence of a large population of DA-1 receptors in this region.
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PMID:Studies on the mechanisms of the development of tolerance to the hypotensive effects of fenoldopam in rats. 245 48

Cromakalim (BRL 34915), a K+ channel activator, and diltiazem relaxed isolated rat aortic rings contracted with a low KCl concentration (25 mM). Gilbenclamide (0.1-3 microM) did not modify base-line resting tension or responses to KCl but prevented the vasorelaxant effects of cromakalim without affecting those of diltiazem or nitrendipine. Cromakalim, in contrast to the latter compounds, did not relax aortic rings contracted with 55 mM KCl. In pentobarbital-anesthetized rats prepared for hemodynamic measurements with Doppler flow probes, a 20-min i.v. infusion of cromakalim (5.0 micrograms/kg/min) lowered mean carotid artery blood pressure. This effect reached maximum after administration and was accompanied by decreases in systemic (35%), hindquarter (45%), mesenteric (27%), and renal (19%) vascular resistances. The blood pressure effects of cromakalim were not modified by BW 755C (lipo and cyclooxygenase inhibitor), idazoxan, methylatropine, methysergide, promethazine, propranolol, SCH 23390 (DA-1 receptor antagonist), S-sulpiride, RP 59227 (antagonist of platelet activating factor receptors) or by bilateral vagotomy associated with ligation of carotid arteries. However, in rats pretreated with the hypoglycemic sulfonylureas glibenclamide or glipizide (20 mg/kg i.v.), cromakalim, in contrast to diltiazem or dihydralazine, failed to produce hypotension. In rats deprived of sympathetic drive by pithing, cromakalim produced only a minor fall in blood pressure; however, this effect became pronounced when the low base-line blood pressure of this preparation was elevated by an i.v. infusion of vasopressin and could be prevented by glibenclamide. In conclusion, cromakalim posseses a novel mechanism of vasorelaxation that is consistent with the activation of a cellular outward K+ current.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasorelaxant effects of cromakalim in rats are mediated by glibenclamide-sensitive potassium channels. 249 53

1. Dose-dependent vasodilator responses to dopamine, isoprenaline, noradrenaline, 3-isobutyl-1-methylxanthine (IBMX) and sodium nitroprusside were obtained in isolated perfused mesentery preparations, taken from reserpine-treated rats of different ages. The preparations were pretreated with phenoxybenzamine (1 microM) and perfused with physiological salt solution containing cocaine (10 microM), additional KCl (20 mM) and vasopressin (0.1 microM). 2. Vasodilator responses to dopamine were abolished by the dopamine1 (DA1)-selective antagonist SCH 23390 (10 nM) and those to isoprenaline by propranolol (1 microM), but the vasodilator responses to noradrenaline were abolished only when SCH 23390 and propranolol were used together. This indicated that dopamine was acting via DA1-receptors, isoprenaline via beta-adrenoceptors and that noradrenaline could act via DA1-receptors and beta-adrenoceptors in this preparation. 3. Responses to all the vasodilator drugs decreased in magnitude between the ages of 1 and 2 months. Responses to dopamine declined further in 4 month-old rats and were negligible at 6 or 22-24 months of age. Responses to isoprenaline were well maintained up to 6 months of age, but were negligible at 22-24 months. 4. It is concluded that, in the rat mesenteric vasculature, there is a non-specific decline in responses to vasodilator drugs during development (1 to 2 months). Subsequently there is a specific decline in DA1-receptor-mediated and beta-adrenoceptor-mediated responses; the former are lost at an earlier age than the latter. This different time course suggests that age influences receptor numbers, or their coupling to adenylate cyclase, rather than a post-receptor event in the adenylate cyclase/cyclic AMP pathway.
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PMID:Vasodilator responses to dopamine in rat perfused mesentery are age-dependent. 280 50

In anaesthetized beagles, saralasin, phentolamine, 1-penicillamine-2-O-methyl-tyrosine-8-arginine-vasopressin and SCH 23390, a DA1 antagonist, were infused into the left renal artery (i.r.a.) and indomethacin and aprotinin intravenously (Group 1). In Groups 2 and 3, i.r.a. infusion of two chemically different putative leukotriene (LT) antagonists, FPL 55712 (100 micrograms/kg/min) and LY 171883 (500 micrograms/kg/min), respectively, was superimposed in the fourth period of experiments. In comparison to Group 1, there was an increase (40% in Group 2 and 33% in Group 3) in renal blood flow and a decrease in glomerular filtration rate (16% and 17%, respectively) and filtration fraction (36% and 41%, respectively). Similar changes were observed on the single nephron level. Directly measured glomerular capillary pressure decreased by 10% and 12%, respectively. A decrease in total arteriolar resistance by 34% and 25%, respectively, was caused by a comparatively higher decrease in efferent (44% and 34%, respectively) than afferent (26% and 15%, respectively) arteriolar resistance values. No change in the ultrafiltration coefficient, Kf, was detected. Providing FPL 55712 and LY 171883 are specific LT antagonists, these experiments suggest a possible constrictory role of LT (expressed more on the efferent than afferent arteriole) in anaesthetised mildly surgically stressed dogs.
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PMID:A possible role for leukotrienes in the regulation of glomerular haemodynamics in the dog. 284 54

This report summarizes studies aimed to characterize pharmacologically, hemodynamically and biochemically DA-1 (fenoldopam) and DA-2 (quinpirole) dopamine receptor agonists in anesthetized rats. Fenoldopam (20 micrograms/kg/min i.v. over 15 min) and quinpirole (10 micrograms/kg/min i.v. over 15 min) share the common property of decreasing mean carotid artery blood pressure by lowering peripheral vascular resistance. Fenoldopam increased mesenteric and renal blood flows whereas quinpirole decreased the former blood flow, but enhanced the latter. These effects of quinpirole were antagonized selectively by S-sulpiride, but not SCH 23390; however, with fenoldopam the reverse was found. In chlorisondamine-pretreated rats with blood pressure supported by vasopressin, fenoldopam, but not quinpirole, caused hypotension. In nephrectomized rats, the blood pressure effects of fenoldopam (assessed as area under the infusion time-response curve) were more pronounced than in sham-operated controls. The hypotensive effects due to an i.v. bolus injection of fenoldopam, but not to acetylcholine, histamine, salbutamol or quinpirole, were significantly inhibited in rats pretreated with an infusion of fenoldopam. In pithed rats, quinpirole reduced the pressor responses to electrical stimulation of the spinal cord without affecting those to exogenous norepinephrine, angiotensin II or 5-hydroxytryptamine which, on the contrary, were inhibited by fenoldopam. The plasma renin activity (in intact rats) was reduced by quinpirole, but elevated by fenoldopam. The latter effect also occurred in pithed rats and was blocked by SCH 23390. Quinpirole lowered heart rate, whilst fenoldopam produced tachycardia. These effects of quinpirole and fenoldopam were significantly inhibited by S-sulpiride and SCH 23390, respectively. In chlorisondamine-pretreated rats quinpirole failed to change heart rate whereas fenoldopam still increased it. In conclusion, these results indicate that DA-1 and DA-2 dopamine receptor agonists can be easily discriminated on the basis of their cardiovascular profiles.
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PMID:Cardiovascular characterization of DA-1 and DA-2 dopamine receptor agonists in anesthetized rats. 288 15


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