Effect of vasopressin on cardiovascular and renal functions and ANP release under plasma volume expansion

To assess the mechanisms whereby arginine vasopressin (AVP) increases atrial natriuretic peptide (ANP) release and to examine whether AVP-mediated ANP release affects the effect of AVP on the cardiovascular and renal function, AVP was infused continuously at a rate of 20 ng.kg-1.min-1 for 75 min following 200 ng/kg bolus injection under stepwise increases in plasma volume in anesthetized dogs. Moreover, the effect of an AVP antagonist, a V1 blocker, 1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-2-(o-methyl)tyrosine AVP (TMeAVP), on these parameters was also investigated. In the control study, saline alone was infused. AVP infusion increased total peripheral resistance (TPR), pulmonary capillary wedge pressure (PCWP), and plasma ANP, but decreased cardiac index (CI) and heart rate (HR) without increases in mean arterial blood pressure (MABP). Stepwise rises in plasma volume further increased plasma ANP, CVP, CI and PCWP, but gradually decreased TPR. TMeAVP curtailed AVP-induced increases in TPR and plasma ANP as well as decreases in CI and HR. The replacement of ANP to prevent a fall in plasma ANP following TMeAVP never affected cardiovascular function. AVP infusion increased plasma volume accompanied by a fall in urinary Na excretion (UNaV) and urine flow (UF) under the stepwise plasma volume expansion compared to the control group, but did not affect mean circulatory filling pressure (MCFP). ANP administration enhanced UNaV and UF and decreased MCFP. These results indicate that AVP may preferentially increases ANP release via the increased cardiac afterload, not preload, but increased plasma ANP per se may not be involved directly in the AVP-induced cardiac suppression.