Hemodynamic effects of exogenous and endogenous vasopressin at low plasma concentrations in conscious dogs.

Abstract

The possibility that vasopressin plays a role in cardiovascular control arouses increasing interest. We studied in unanesthetized dogs the hemodynamic consequences of 1-hour vasopressin infusions that modified plasma concentrations over a range similar to that found in physiological situations. We also examined the cardiovascular events following the stimulation of endogenous vasopressin release by an increase in plasma osmolality. In dogs with baroreceptor reflexes intact, vasopressin infusions which increased plasma vasopressin concentration by 2-20 fmol/ml did not affect mean arterial pressure. However, they significantly decreased cardiac ouput (measured by an electromagnetic flowmeter) and increased total peripheral resistance. After baroreceptor denervation, vasopressin infusion rates as low as 40 fmol/kg per min (0.017 microU/kg per min) led to an increase in mean arterial pressure. Cardiac output was unaffected until much higher infusion rates were used. Changes in total peripheral resistance were very similar to those calculated in dogs with intact baroreceptors. The release of vasopressin following infusions of hypertonic solutions either intravenously or into a carotid artery induced detectable hemodynamic changes which appeared in many respects similar to those following low infusion rates of vasopressin. We conclude that physiological plasma concentrations of vasopressin have hemodynamic effects even though they do not normally modify arterial pressure, presumably because of some particular interaction of vasopressin with the baroreceptor reflex.

Effect of methadone on plasma arginine vasopressin level and urine production in conscious dogs

“…In agreement with investigations which incorporated extensive circulatory monitoring, the relative bradycardia can be at least partially accounted for by the increased AVP level (Malayan et al, 1980;Montani et al, 1980;Liard et al, 1981;Undesser et al, 1985). These reports show that when plasma AVP levels are increased to an extent comparable with the levels reached in this experiment, there is an increase in total peripheral resistance without concurrent increase in mean arterial pressure.…”

“…These reports show that when plasma AVP levels are increased to an extent comparable with the levels reached in this experiment, there is an increase in total peripheral resistance without concurrent increase in mean arterial pressure. This is caused by a fall in cardiac output which is postulated to be centrally mediated through direct interaction of AVP with the central nervous system structures, possibly involving baroreceptor reflex pathways (Montani et al, 1980;Liard et al, 1981). Furthermore, the parasympathomimetic effect of methadone causes a decrease in heart rate (Hall and Clark, 1983).…”

Plasma vasopressin, renin and catecholamines during nitroprusside-induced hypotension in the newborn lamb

“…These results are in agreement with those of ROSE et al and KUIPERS et al, in the newborn lamb but not with those of Ross et al in the fetal lambs where a tachycardia was observed [20,27,30]. These differences could be due to differences in rates of infusion, age of the lambs and to the negative chronotropic effects of high levels of vasopressin found in ROSE'S and our experiments but not in those of Ross [23,27,30]. During nitroprusside induced hypotension, plasma levels of vasopressin of the newborn lamb rose 15 fold, plasma renin activity 4 fold and catecholamines 3 fold (figure 2).…”

Changes in Plasma Vasopressin Levels and Cardiovascular Function due to Postural Changes in Diabetic Neuropathy.

“…Indeed, Zerbe et al (1981Zerbe et al ( , 1983 reported that plasma AVP increased markedly in response to decreased blood pressure in normal subjects (50 to 500 pg/ml). Moreover, in animal studies, increases of at least more than 50 pg/ml in plasma AVP have been reported to be necessary to increase blood pressure (Montani et al 1980;Mohring et al 1981). Reid et al (1989) reported that impairment of AVP release in diabetic neuropathy was not due to impaired AVP release from the pituitary gland, because the AVP response to osmotic stimuli has been reported not to be impaired.…”