Abstract
The role of the adrenal cortex in the pathogenesis of ascites has been studied in adrenalectomized dogs with thoracic inferior caval constriction. Discontinuation of hormone therapy resulted in a diuresis which demonstrates that adequate adrenocortical function or replacement therapy is essential for ascites formation during normal sodium (Na) intake. Evidence is presented in support of the thesis that sodium retention results from an excess of circulating adrenocortical salt-retaining hormones.
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