SUMMARYThe effects of physiological elevations in arginine vasopressin on the cardiovascular system were studied in a group of nine conscious, chronically instrumented dogs. The animals were studied under normal conditions (plasma vasopressin, 4.1 ± 0.4 pg/ml), after 24 hours of dehydration (plasma vasopressin, 7.3 ±1.5 pg/ml), after a 30-minute vasopressin infusion at 2.6 ng/kg/min (plasma vasopressin, 62.8 ± 10.3 pg/ml), and after a 4-day vasopressin infusion at 2.6 ng/kg/min (plasma vasopressin, 96.6 ±8.1 pg/ml). These increases in vasopressin concentration resulted in no change in arterial pressure and significant changes in the following: a 13 and 29% decrease in resting cardiac output during dehydration and acute infusion, respectively; a 26% reduction in heart rate during acute infusion; a 12 and 54% increase in total peripheral resistance during dehydration and acute infusion; a 16 and 22% reduction in mean circulatory filling pressure during dehydration and chronic vasopressin infusion. In addition, maximum pumping ability of the heart was reduced 16 and 31 % during dehydration and acute infusion, respectively. These data suggest that elevations of vasopressin such as those occurring during dehydration or volume depletion potentially may affect cardiovascular performance by three mechanisms: 1) greatly increasing resistance to flow, 2) reducing heart rate, 3) suppressing the pumping ability of the heart. A LTHOUGH the pressor capabilities of arginine /\ vasopressin (AVP) have been recognized A. JL. since 1895, the physiological role of the hormone in cardiovascular regulation remains controversial (for reviews of this subject, see References 1 and 2). In normal, conscious animals or humans, elevations in AVP concentration into the high physiological range bring about small increases in arterial pressure, in cardiovascular regulation, the results of other recent studies raise the possibility that AVP may be important in cardiovascular control, at least in some conditions. Some of the more provocative data have come from the studies of Cowley et al. 3 and Montani et al., 3 who showed that, although changes in plasma AVP concentration within the physiological range do not produce large cardiovascular alterations in intact animals, the same increases of AVP concentration in baroreceptordenervated animals or patients with impaired cardiovascular reflexes 4 have prominent cardiovascular and hemodynamic effects. Therefore, these studies suggest that in the intact animals some aspect of baroreceptor function masks the cardiovascular effects of AVP. Additionally, administration of antagonists to the vascular receptor in several experimental models of hypertension 7 "9 and during hemorrhage 10 results in transient decreases in peripheral resistance and arterial pressure. These findings suggest that AVP is an active element of cardiovascular regulation, at least in some pathophysiological conditions.Previous analyses of the effects of AVP on the cardiovascular system have dealt mainly with the effects of the hormo...