Renal-Adrenal Relationships in Hypertension

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FOLLOWING my training with Dr. Hans Selye, when I became associated with Doctors Page and Corcoran in 1948, my interest understandably was directed system had been identified and was believed by many to be the main pathogenic factor in renal and clinical hypertension. Desoxycorticosterone acetate (DCA), then a hypothetic hormone, was known to elicit hypertension when given to salt-treated rats. Although renal hypertension and DCA hypertension were considered different entities, there were indications they might have some mechanisms in common. Renal hypertension was associated with an increase in adrenal weight, and DCA hypertension, according to some investigators, with an activation of the renal pressor system, because of the presence of nephrosclerosis. With this background, I shall summarize the experiments that have led us to a new concept of renal-adrenal relationships in hypertension, which has proved useful as a working hypothesis.

Our first experiment was based on the assumption that the renal pressor system, not stress, was responsible for adrenal stimulation noted during renal hypertension. In spite of the belief that renin formed antibodies and was active only when administered intravenously, we injected various renal extracts subcutaneously into rats over a period of several weeks. Only extracts possessing pressor activity caused diuresis and proteinuria, effects previously recognized in acute experiments. Animals lost weight as had been noted in malignant hypertension, and their adrenals showed hypertrophy of the zona glomerulosa, which is considered the site of formation of desoxycorticosterone (DC)-like steroids. Similar adrenal changes were noted in rats with renal hypertension. At . . .