Systemic and regional hemodynamic effects of endogenous vasopressin stimulation in rats

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Abstract
Systemic and regional hemodynamic alterations induced in normotensive anephric rats, were investigated by stimulation of endogenous vasopressin with an acute Na and fluid load, as well as those following vasopressin inhibition with a specific antagonist [1-(.beta.-mercapto-.beta.,.beta.-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine-arginine vasopressin] of its vasoconstricting action were investigated. Blood pressure and total peripheral resistance were significantly higher and cardiac output was lower in rats with stimulated vasopressin, and all were reversed to near control levels in rats receiving the vasopressin inhibitor. Regional blood flows were diminished in most organs and local vascular resistance was elevated compared with control animals, but the magnitude of change varied widely. Heart blood flow did not decrease significantly and brain blood flow actually increased indicating small or no change in vascular resistance of these organs. Fractional distribution of the diminished cardiac output to these organs was significantly higher, so that blood flow to vital organs was maintained at the expense of blood flow to other tissues. In rats that received the vasopressin antagonist after the saline infusion, regional blood flows were similar to those of control animals. Blood pressures at the baseline and after hypertonic NaCl infusion correlated closely with the corresponding plasma levels of control and stimulated vasopressin.