We measured plasma arginine vasopressin (AVP) and plasma renin activity (PRA) during continuous hemorrhage in cardiac-denervated and sham-operated conscious dogs. Hemorrhage produced comparable decreases in aortic pressure, cardiac output, stroke volume, pulmonary arterial pressure, and left and right atrial pressures in each group of dogs. After 10 ml blood/kg body wt had been removed, AVP was increased in sham-operated dogs (P less than 0.05) but not in cardiac-denervated dogs. After 20 and 30 ml blood/kg body wt had been removed, AVP was increased in all dogs, but the response was markedly attenuated in cardiac-denervated dogs. Hemorrhage at 10 and 20 ml/kg caused comparable increases in PRA in each group of dogs. However, at 30 ml/kg hemorrhage the increase in PRA was significantly higher in cardiac-denervated dogs than in sham-operated dogs. Our results suggest that cardiac receptors play a dominant role in mediating the release of AVP during hemorrhage in conscious dogs. In contrast, we found no evidence for a dominant role of cardiac receptors in mediating renin secretion during hemorrhage.

These experiments were designed to investigate whether a reflex arising from ventricular receptors is capable of stimulating vasopressin secretion during hemorrhage. Three groups of conscious dogs (sham operated, cardiac denervated, and ventricular denervated) were hemorrhaged slowly until 30 ml blood/kg body wt had been removed. Hemorrhage produced comparable decreases in stroke volume, central venous pressure, and left atrial pressure in each group of dogs but produced a different pattern of heart rate response in each group. Plasma vasopressin concentrations before hemorrhage did not differ in the three groups of dogs. In sham-operated dogs plasma vasopressin increased from a control level of 2.4 +/- 0.3 to 6.2 +/- 1.7, 200.0 +/- 65.4, and 991.3 +/- 220.9 pg/ml after 10, 20, and 30 ml/kg of blood had been removed, respectively. In contrast, plasma vasopressin did not increase in either cardiac-denervated or ventricular-denervated dogs after 10 ml/kg of blood had been removed, and the increases in circulating vasopressin after 20 and 30 ml/kg hemorrhage were markedly attenuated by cardiac denervation and by ventricular denervation. The magnitude of the increase in plasma vasopressin in the cardiac-denervated and ventricular-denervated dogs did not differ significantly at comparable levels of hemorrhage. The results are consistent with the possibility that a reflex initiated by ventricular receptors is primarily responsible for stimulating the secretion of vasopressin during hemorrhage in conscious dogs.