Cardiovascular effects of vasopressin following V₁ receptor blockade compared to effects of nitroglycerin

Abstract

Studies to more clearly determine the mechanisms associated with arginine vasopressin (AVP)-induced vasodilation were performed in normal subjects and in quadriplegic subjects with impaired efferent sympathetic responses. Studies to compare the effects of AVP with the hemodynamic effects of nitroglycerin, an agent that primarily affects venous capacitance vessels, were also performed in normal subjects. Incremental infusions of AVP following V(1)-receptor blockade resulted in equivalent reductions in systemic vascular resistance (SVRI) in normal and in quadriplegic subjects. However, there were major differences in the effect on mean arterial pressure (MAP), which was reduced in quadriplegic subjects but did not change in normal subjects. This difference in MAP can be attributed to a difference in the magnitude of increase in cardiac output (CI), which was twofold greater in normal than in quadriplegic subjects. These observations are consistent with AVP-induced vasodilation of arterial resistance vessels with reflex sympathetic enhancement of CI and are clearly different from the hemodynamic effects of nitroglycerin, i.e., reductions in MAP, CI, and indexes of cardiac preload, with only minor changes in SVRI.

Acute Changes in Systemic Hemodynamics and Serum Vasopressin After Complete Cervical Spinal Cord Injury in Piglets

“…In individuals with chronic SCI, diurnal variation in serum AVP concentration is attenuated and can lead to nocturnal enuresis, which is effectively treated with exogenous vasopressin [46,47]. The vasoconstrictive actions of AVP are well known; however, AVP also has vasodilatory properties at least in part via activation of vasopressin-2 (V 2 ) receptors, as hypotension has been observed in individuals with chronic quadriplegia after administration of a V 1 receptor antagonist [39,40,48,49]. This study is the first to measure acute changes in serum AVP concentration in response to SCI.…”

Vasopressin and epinephrine in the treatment of cardiac arrest: an experimental study

“…Via the V 1 receptors, it stimulates the contraction of vascular smooth muscles, resulting in peripheral vasoconstriction and increased blood pressure. Via the V 2 receptors, vasopressin possibly induces vasodilation [ 21 - 23 ]. Unlike epinephrine, it is resistant to the effects of acidosis [ 24 , 25 ].…”

G-Protein-coupled receptors as potential drug candidates in preeclampsia: targeting the relaxin/insulin-like family peptide receptor 1 for treatment and prevention

“…That is, hydrolysis of AVP at the Cys-Tyr bond by vasopressinase precludes interaction with the V2 receptor by breaking the ring structure, while preserving the N terminus required for V1 activity. Earlier studies in rats, dogs and humans demonstrate that AVP is vasodilatory in the setting of V1 blockade, illustrating the opposing vascular actions of these two receptor subtypes (Glanzer et al, 1982;Liard, 1986;Walker, 1986;Naitoh et al, 1993;Cooke et al, 2001). Thus, it is not inconceivable that unopposed V1 activation by 'vasopressinase altered vasopressin' could promote vasoconstriction, platelet aggregation and endothelial dysfunction.…”