Escape from Sodium-Retaining Effects of Deoxycorticosterone in Hypotensive and Hypertensive Dogs

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Abstract
The ability of the mammalian kidney to escape from the sodium-retaining effects of mineralocorticoid hormones has not been thought to depend upon increases in blood pressure or renal perfusion. However, chronic exposure to excess endogenous or exogenous adrenal cortical hormones results in hypertension, and it seemed possible that early small increments in blood pressure might play a role in escape. To evaluate this, hypotension was produced with drugs in dogs, and their ability to escape was studied. A combination of hydralazine and guanethidine effectively lowered blood pressure but did not prevent or delay renal escape from deoxycorticosterone. Production of hypotension after escape resulted in sodium retention for 1 day, but then sodium balance resumed despite continued hypotension and lowered renal blood flow and filtration. Mean arterial blood pressure in dogs with thoracic inferior vena caval constriction was not significantly below normal, and elevation of blood pressure with ephedrine failed to increase sodium excretion or permit renal escape from deoxycorticosterone. These studies indicate that neither increased blood pressure nor α-adrenergic tone is necessary for renal escape from the salt-retaining effects of mineralocorticoid hormones.

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