Abstract
Passive venous congestion of the liver following constriction of the inferior vena cava above the hepatic veins impairs the renal excretion of sodium and water loads, and greatly increases the responsiveness of rats to the sodium-retaining and life-maintenance effects of desoxycorticosterone. These experiments support the hypothesis that the in vivo rate of inactivation of adrenal cortical hormones may be impaired by central passive venous congestion, and suggest the possibility that the secondary aldosteronism of congestive heart failure may be accounted for in part by a defect in steroid metabolism.

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