Analysis of the cardiovascular effects of arginine vasopressin in conscious dogs.

Abstract

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...

Arginine Vasopressin Infusion Increases Plasma Levels of Atrial Natriuretic Factor in Humans

“…These results are in agreement with a study carried out in conscious dogs using doses of AVP similar to those used in our study (Tipayamontri, Young, Nuwayhid and Scott 1987). The discordant results between our study and previous studies in humans (Aylward et al 1986) may be related to the higher doses of AVP used by these authors.…”

Effect of Vasopressin on Cardiovascular and Renal Functions and ANP Release under Plasma Volume Expansion.

“…Thirdly, it is likely that either increased TPR may rise cardiac afterload leading to a fall in cardiac output and/or increased RVR may decrease venous return with ensuring the reduction in cardiac output. Indeed, Tipayamontri et al (1987) reported that AVP increased both RVR and TPR, leading to a fall in cardiac output in dogs. Therefore, taken together, it appears likely that all the mechanisms above-mentioned may be possible explanations for the hypoeffective heart observed in the present study as shown in Fig.…”

Haemodynamic and Humoral Consequences of Chronic Infusion of Vasopressin in Conscious Rats

“…In addition, AVP seems to retain a long-term vasoconstrictor effect, since the injection of VI antagonist decreased total peripheral resistance and increased cardiac output and heart rate. In additional studies, 4-day infusions of AVP failed to alter arterial pressure or total peripheral resistance in spite of the marked elevation of plasma AVP concentration to 97 pg/ mL (Tipayamontri et al 1987). Thus, the haemodynamic consequences of chronic AVP infusion may vary with the experimental conditions.…”

“…To determine whether chronic excess of AVP produces persistent elevation of arterial pressure, the long-term effects of exogenous infusion of AVP have been investigated (Brown et al 1986;Cowley et al 1986;Hall et al 1986;Liard 1987;Tipayamontri et al 1987). Although most of these experiments revealed the persistent vasoconstrictor and/or antidiuretic effects of AVP, the ability of AVP to produce sustained elevation of arterial pressure was not demonstrated consistently.…”