Mechanisms regulating neurohypophysial blood flow and function during isotonic volume expansion

Regional cerebral and neurohypophysial blood flow responses to isotonic extracellular fluid volume expansion were studied in pentobarbital-anesthetized dogs using radiolabeled microspheres. Measurements were made at baseline and after increasing pulmonary capillary wedge pressure by 8 +/- 2 mmHg. Plasma arginine vasopressin (AVP) decreased by 50%, and neural lobe blood flow (NLBF) decreased by 47%. Blood flow through median eminence and other brain regions was unchanged. We investigated potential mechanisms responsible for the NLBF changes. Following control vagotomy, AVP concentration increased during the first hour and then returned to control values for hours 2 and 3, whereas NLBF was unchanged for the first hour and fell after 2 and 3 h. Vagus section abolished the decrease in NLBF but not the AVP response to volume expansion. The contribution of left atrial and pulmonary baroreceptors to this response was tested by inflation of a balloon in the left atria to produce a 13 +/- 1 mmHg rise in atrial pressure. This led to a 20% reduction in NLBF, a 35% reduction in AVP concentration, and a 270% increase in plasma atrial natriuretic factor (ANF). However, ANF release does not account for the NLBF changes, since intravenous ANF infusion had no effect on NLBF or AVP concentration. These data suggest that the NLBF response to volume expansion is mediated by the vagus with input from multiple cardiopulmonary baroreceptors.