Effects of vasopressin V1-receptor blockade during acute and sustained hypovolemic hypotension.

The response of vasopressin and its role in the maintenance of arterial pressure during and after development of hypotensive central hypovolemia were studied in tilt table studies in quadriplegic subjects. The studies were performed during acute head-up tilting to a maximally tolerated degree of tilt (8 subjects) and during sustained head-up tilt following a 20% reduction in mean arterial pressure (MAP) (11 subjects). Studies in all subjects were performed on two separate days, once with and once without administration of a selective vasopressin V1-receptor antagonist. During acute head-up tilting, plasma vasopressin concentrations (PAVP) did not increase significantly until MAP decreased to approximately 60 mmHg at maximal tilt. There was no difference in the degree of hypotension produced in the presence compared with the absence of V1-receptor blockade. There was also no difference in plasma renin activity (PRA) or in plasma cortisol or aldosterone concentrations at maximal tilt. In contrast, during sustained head-up tilt following a 20% reduction in arterial pressures, systolic and mean arterial pressures were significantly lower and PRA was significantly higher in the presence than in the absence of V1-receptor blockade. PAVP increased and was significantly higher after 30 min of sustained tilt than pretilt PAVP in supine posture. These studies do not provide evidence of a role for vasopressin in the maintenance of arterial pressure during the acute development of hypotensive hypovolemia in human subjects, but they do provide evidence of a modest role for vasopressin in the maintenance of arterial pressure when the effect of hypovolemia is more moderate and sustained.