Vasopressin Antagonist

2020 ◽  
Author(s):  
Keyword(s):  
Vasopressin Antagonist

Antidiuretic antagonism and agonism of 1-deamino-pentamethylene-2-d-phenylalanine-4-isoleucine-arginine vasopressin in rats with diabetes insipidus

1987 ◽  
Vol 112 (3) ◽  
pp. 439-442 ◽  
Author(s):  
H. Vilhardt ◽  
S. Lundin
Keyword(s):  
Diabetes Insipidus ◽  
Arginine Vasopressin ◽  
Test Model ◽  
Brattleboro Rats ◽  
Experimental Conditions ◽  
Vasopressin Antagonist ◽  
Agonist Action

ABSTRACT Using implanted minipumps it was shown over a period of 7 days that the vasopressin antagonist, 1-deamino-pentamethylene-2-d-Phe-4-Ile-arginine vasopressin, caused increased diuresis in normal rats and reversed vasopressin- or oxytocin-induced antidiuresis in Brattleboro rats. When the antagonist was infused alone in Brattleboro rats it induced a marked antidiuretic response, indicating that the analogue also possessed agonistic properties. The agonist action could not be demonstrated in anaesthetized, hydrated normal rats. In these animals the analogue behaved as a pure antagonist. It is concluded that analogues which behave as antagonists in one test model may display agonistic properties under different experimental conditions. J. Endocr. (1987) 112, 439–442

Vasodepressor action of angiotensin in conscious chickens

1982 ◽  
Vol 243 (3) ◽  
pp. H456-H462 ◽  
Author(s):  
Y. Nakamura ◽  
H. Nishimura ◽  
M. C. Khosla
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Direct Action ◽  
Angiotensin Receptors ◽  
Ang Ii ◽  
Prostaglandin Synthetase ◽  
Vasopressin Antagonist ◽  
Native Chicken ◽  
Blood Pressure Responses ◽  
Depressor Action

In chronically cannulated conscious chickens, Gallus gallus, native chicken angiotensin II ([Asp1,Val5]ANG II) caused biphasic blood pressure responses, a depressor followed by a pressor response. The pressor response appears to be mediated primarily by catecholamines. The depressor responses increased with increasing doses and were accompanied by tachycardia. The onset of the depressor action of [Asp1,Val5]ANG II (2.49 +/- 0.22 s) was nearly as quick as that of acetylcholine or histamine. Replacement of aspartic acid in position 1 with sarcosine or asparagine reduced both depressor and pressor potencies, whereas there was no difference either in depressor or pressor potencies between [Asp1,Val5] and [Asp1,Ile5]ANG II. The depressor response to [Asp1,Val5]ANG II was not inhibited by atropine, a vasopressin antagonist, prostaglandin synthetase inhibitors, methysergide, or propranolol but was blocked markedly by [Sar1, Ile8]ANG II and partially by [Sar1,Thr8]ANG II. The results suggest that the vasodepressor action of ANG II is mediated by angiotensin receptors and may possibly be a direct action on the vascular smooth muscle.

PHARMACOLOGICAL PROFILE OF ORALLY ADMINISTERED YM087, A VASOPRESSIN ANTAGONIST, IN CONSCIOUS RATS

1999 ◽  
Vol 26 (5-6) ◽  
pp. 399-403 ◽  
Author(s):  
Yuichi Tomura ◽  
Atsuo Tahara ◽  
Junko Tsukada ◽  
Takeyuki Yatsu ◽  
Wataru Uchida ◽  
...  
Keyword(s):  
Pharmacological Profile ◽  
Vasopressin Antagonist ◽  
Conscious Rats

A vasopressin antagonist can reverse dominant/subordinate behavior in hamsters

1986 ◽  
Vol 38 (1) ◽  
pp. 135-138 ◽  
Author(s):  
Craig F. Ferris ◽  
David M. Meenan ◽  
John F. Axelson ◽  
H.Elliott Albers
Keyword(s):  
Vasopressin Antagonist

Role of angiotensin and vasopressin on blood pressure of ganglionic blocked dogs

1983 ◽  
Vol 244 (1) ◽  
pp. H115-H120 ◽  
Author(s):  
P. C. Houck ◽  
M. J. Fiksen-Olsen ◽  
S. L. Britton ◽  
J. C. Romero
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Vasopressin Antagonist ◽  
Ganglionic Blockade ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Group 2 ◽  
Group 1

This study was designed to investigate the possible role of angiotensin and vasopressin in the maintenance of arterial blood pressure during acute blockade of the autonomic nervous system. Two groups of eight dogs each were anesthetized with pentobarbital sodium, and autonomic ganglia were blocked with hexamethonium (20 mg/kg). Thirty minutes later group 1 received the vasopressin antagonist 1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine arginine vasopressin (10 micrograms/kg) followed after a 30-min interval by captopril (1 mg/kg). Group 2 received the same drugs, except the order of administration of vasopressin antagonist and captopril was reversed. Vasopressin antagonist during ganglionic blockade (group 2) produced a greater fall in blood pressure than did captopril during ganglionic blockade (group 1). These data indicate that vasopressin plays a greater pressor role than angiotensin in the acute response to ganglionic blockade. Additional studies were performed to determine if the autonomic nervous system alone can support the resting blood pressure in the anesthetized dog. Combined blockade of angiotensin and vasopressin without autonomic blockade produced a significant decrease in blood pressure, suggesting that the autonomic nervous system alone is not able to support the control blood pressure in the anesthetized dog.

Vasopressin and angiotensin II in reflex regulation of ACTH, glucocorticoids, and renin: effect of water deprivation

1992 ◽  
Vol 263 (4) ◽  
pp. R762-R769 ◽  
Author(s):  
V. L. Brooks ◽  
L. C. Keil
Keyword(s):  
Angiotensin Ii ◽  
Water Deprivation ◽  
Adrenocorticotropic Hormone ◽  
Renin Secretion ◽  
Ang Ii ◽  
Elevated Plasma ◽  
Plasma Acth ◽  
Vasopressin Antagonist ◽  
Acth Concentration ◽  
V2 Antagonist

Angiotensin II (ANG II) and vasopressin participate in baroreflex regulation of adrenocorticotropic hormone (ACTH), glucocorticoid, and renin secretion. The purpose of this study was to determine whether this participation is enhanced in water-deprived dogs, with chronically elevated plasma ANG II and vasopressin levels, compared with water-replete dogs. The baroreflex was assessed by infusing increasing doses of nitroprusside (0.3, 0.6, 1.5, and 3.0 micrograms.kg-1.min-1) in both groups of animals. To quantitate the participation of ANG II and vasopressin, the dogs were untreated or pretreated with the competitive ANG II antagonist saralasin, a V1-vasopressin antagonist, or combined V1/V2-vasopressin antagonist, either alone or in combination. The findings were as follows. 1) Larger reflex increases in ANG II, vasopressin, and glucocorticoids, but not ACTH, were produced in water-deprived dogs compared with water-replete dogs. 2) ANG II blockade blunted the glucocorticoid and ACTH responses to hypotension in water-deprived dogs, but not water-replete dogs. In contrast, vasopressin blockade reduced the ACTH response only in water-replete dogs. 3) Vasopressin or combined vasopressin and ANG II blockade reduced the plasma level of glucocorticoids related either to the fall in arterial pressure or to the increase in plasma ACTH concentration in water-replete dogs, and this effect was enhanced in water-deprived dogs. 4) In both water-deprived and water-replete animals, saralasin and/or a V1-antagonist increased the renin response to hypotension, but a combined V1/V2-antagonist did not. These results reemphasize the importance of endogenous ANG II and vasopressin in the regulation of ACTH, glucocorticoid, and renin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasopressin and autonomic mechanisms mediate cardiovascular actions of central serotonin

1991 ◽  
Vol 260 (6) ◽  
pp. R1188-R1193 ◽  
Author(s):  
P. E. Pergola ◽  
R. H. Alper
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Intracerebroventricular Administration ◽  
Vasopressin Antagonist ◽  
Conscious Rats ◽  
Cardiovascular Actions ◽  
Combined Pretreatment ◽  
Hormone Antagonists ◽  
Ly 53857 ◽  
Lateral Cerebral Ventricle

Intracerebroventricular administration of serotonin (5-HT) to conscious rats increases mean arterial pressure (MAP) and decreases heart rate. To determine the mechanisms involved, 5-HT (2.5 micrograms) was injected intracerebroventricularly into conscious rats pretreated with various neurotransmitter and hormone antagonists. The selective 5-HT2 antagonist LY 53857 abolished the increase in MAP and the bradycardia elicited by 5-HT. The increase in MAP produced by 5-HT was potentiated by chlorisondamine (a ganglionic antagonist), unaffected by prazosin (an alpha 1-antagonist) or a vasopressin V1 antagonist alone, but eliminated by the combined pretreatment with prazosin plus the vasopressin antagonist. In contrast, the bradycardia was eliminated by either the vasopressin V1 antagonist or chlorisondamine. In conclusion, 5-HT injected into the lateral cerebral ventricle of conscious rats induces sympathoexcitation and the release of vasopressin, which results in an increase in MAP; 5-HT also elicits a bradycardia mediated through an interaction of the autonomic nervous system with circulating vasopressin.

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