The role of the adrenal cortex in the pathogenesis of hypertensive cardiovascular-renal disease has long been the subject of scientific debate. However, as a result of recent observations on the therapeutic effect of bilateral adrenalectomy in a small number of hypertensive patients,* the presence of increased quantities of aldosterone in the urine of patients with essential hypertension,† and the production of experimental hypertension with aldosterone,‡ the question no longer seems to be whether or not the adrenal cortex participates in the genesis of certain forms of this disease but rather how the adrenal cortex participates. That it is probably not through a simple "derailment" of the response to nonspecific stress, as originally proposed by Selye,9 has been shown by the observation that, with the single exception of cold, nonspecific stress has been notably unsuccessful in reproducing hypertension and vascular lesions in the experimental animal.10 The complexity of adrenal
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