Vasopressin reduces oxygen uptake in intact dogs but not in sinoaortic-denervated dogs

Abstract

We have investigated the effect of infusions of arginine vasopressin on cardiac output and O2 uptake in the presence and in the absence of sinoaortic reflexes to better understand the mechanism of the exaggerated decrease in cardiac output elicited by vasopressin. Chronically instrumented dogs received, on separate days, 30-min infusions of vasopressin (0.2, 1, 5, 20, and 60 ng.kg-1.min-1), phenylephrine (1, 3, and 10 micrograms.kg-1.min-1), and angiotensin II (ANG II) (10, 20, and 50 ng.kg-1.min-1). These infusions all increased mean arterial pressure to a maximum of 63 +/- 8.2 mmHg during the highest phenylephrine infusion rate. Vasopressin reduced cardiac output (electromagnetic flowmeter) more than the other vasoconstrictors for equivalent increases in arterial pressure. Vasopressin also produced dose-dependent decreases in O2 uptake, measured by collection of expired air. Such decreases were not observed with the other two agents. On the contrary, ANG II and phenylephrine increased O2 uptake significantly when they decreased cardiac output the most. The decrease in O2 uptake induced by vasopressin was significantly correlated with the decrease in cardiac output. Pretreatment of the dogs with atropine prevented the decrease in O2 uptake and blunted the fall in cardiac output induced by vasopressin at a rate of 5 ng.kg-1.min-1. In dogs surgically deprived of sinoaortic receptors, vasopressin given at 1 and 5 ng.kg-1.min-1 failed to reduce O2 uptake and cardiac output significantly.(ABSTRACT TRUNCATED AT 250 WORDS)