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The effects of infusions of arginine vasopressin or 1‐deamino‐8‐D‐arginine vasopressin on common carotid vascular resistance in conscious, Long Evans rats
Author(s) -
Gardiner S.M.,
Compton A.M.,
Bennett T.
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb11936.x
Subject(s) - vasopressin , medicine , vascular resistance , blood pressure , vasopressin receptor , vasodilation , vasopressin antagonists , endocrinology , heart rate , perfusion , anesthesia , circulatory system , antagonist , receptor
1 Intravenous infusions of arginine vasopressin or 1‐deamino‐8‐ d ‐arginine vasopressin (DDAVP) were given to conscious, Long Evans rats chronically instrumented with bilateral, common carotid, pulsed Doppler probes and intravascular catheters. 2 During infusion of vasopressin at 0.3 nmol min −1 there was an increase in common carotid vascular resistance with no change in mean blood pressure or heart rate. Following infusion there was a common carotid vasodilatation. 3 During infusion of vasopressin at 3.0 nmol min −1 there were increases in mean arterial blood pressure and in common carotid vascular resistances, accompanied by bilateral reductions in flow and in heart rate. Administration of (+)−(CH 2 ) 5 Tyr(Et)DAVP (a V 1 ‐receptor antagonist), during the continued infusion of vasopressin, reversed the effects of the latter on mean blood pressure and heart rate; under these conditions there were increases in common carotid blood flows above baseline, in company with bilateral vasodilatations. The latter effects persisted after cessation of vasopressin infusion. 4 Infusions of DDAVP were without significant effects on any measured cardiovascular variable. 5 The results do not provide straightforward support for the claim that vasopressin acts to promote cerebral perfusion, at least when V 1 ‐receptor effects are unopposed. Furthermore, it seems likely that the vasodilator influence of vasopressin on the common carotid vascular bed is not due to stimulation of V 2 ‐receptors.