Hemodynamic, hormonal, and drinking responses to reduced venous return in the dog.

Abstract

The effect of an acute reduction in venous return, caused by reversible constriction of the thoracic vena cava, on drinking and secretion or arginine vasopressin (AVP) was examined in the dog. Plasma AVP levels rose immediately from a control level of 1.4 +/- 0.1 pg/ml (mean +/- SE) to a plateau ranging between 36 and 42 pg/ml during the first 30 min after constriction but declined to 12.6 +/- 4.2 pg/ml 2 h after constriction even though systemic arterial hypotension was maintained. Drinking occurred with a latency of 22 +/- 6 min and 13.2 +/- 1.8 ml H2O/kg was consumed during 2 h of vena caval constriction. Water intake was significantly correlated with the average reduction in blood pressure (r = 0.86; n = 8; P less than 0.01) but not with plasma renin activity. The role of angiotensin II (ANG II) in the drinking and secretion of AVP in response to decreased venous return was evaluated using the ANG II receptor blocker, saralasin, infused intravenously (iv) or intracerebroventricularly (icv). Intravenous, but not icv, infusion of saralasin during vena caval constriction reduced the ability of the dogs to maintain arterial blood pressure (P less than 0.05). However, neither iv nor icv saralasin significantly affected water intake or the rise in plasma AVP in response to vena caval constriction when compared to their respective controls. Taken together, these data show that angiotensin is important in the maintenance of systemic arterial blood pressure but is not essential for the rise in plasma AVP or drinking in response to an acute reduction in venous return. It is suggested that either arterial baroreceptors or "low-pressure" volume receptors or both mediate the drinking and AVP responses in the presence of central blockade of the effects of circulating angiotensin.