Abstract
As a result of the work of Goldblatt and his associates,1 emphasis has been placed in recent years on the role of the kidney in the pathogenesis of both experimental and essential hypertension. However, the absence of recognizable signs of impaired renal function or of significant anatomic change early in the course of hypertensive vascular disease has been advanced as an argument against renal ischemia as the primary cause of this disorder in man.2 There is considerable evidence that the adrenal cortex plays a part in the regulation of the arterial blood pressure. Hypertension may be a manifestation of certain adrenal cortical tumors, and hypotension is a frequent observation in Addison's disease even after restoration of electrolyte and water balance by appropriate therapy. Desoxycorticosterone acetate has been found capable of producing hypertension in some patients with hypoadrenalism and of raising the blood pressure in others without renal or

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