Role of vasopressin in cardiovascular and neurohormonal responses to intracerebroventricular hypertonic NaCl.

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Abstract
To determine the significance of vasopressin in cardiovascular and neurohormonal responses caused by centrally administered hypertonic NaCl, we examined the effects of a vasopressin antagonist on blood pressure, heart rate, plasma levels of catecholamines, cortisol and renin activity in anesthetized dogs. Intracerebroventricular (ICV) injections of 0.2 ml of 1.5 M NaCl increased mean arterial blood pressure (+29.7 .+-. 3.0 mmHg, mean.+-.SE), heart rate (+27.9 .+-. 7.0 beats/min), plasma concentrations of vasopressin (+48.9 .+-. 8.2 pg/ml), norepinephrine (+40.0 .+-. 6.2 pg/ml), epinephrine (+231.4 .+-. 21.4 pg/ml) and cortisol (+5.3.+-.1.1 .mu.g/dl) and decreased plasma renin activity (-2.0 .+-. 0.4 ng/ml/hr). An intravenous vasopressin antagonist, d(CH2)5Tyr(Me)AVP, at a dose at 10 .mu.g/kg, attenuated the pressor response and augmented the heart rate exposure to ICV 1.5 M NaCl. The vasopressin antagonist also augmented the change in plasma norepinephrine and significantly attenuated the responses of cortisol and renin. Baseline levels of these variables were not altered by the vasopressin antagonist except for an increase in renin activity. Two injections of hypertonic NaCl without any pretreatment produced similar cardiovascular and hormonal responses. These results suggest that vasopressin contributes not only to an increase in blood pressure, but also in changes in the sympathetic nervous system, the hypothalmao-adrenocortical axis and the peripheral renin-angiotensin system in response to a central sodium stimulus.

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