Adrenocortical Hormones in Human Hypertension and Their Relation to Angiotensin

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Abstract
In summary, we have demonstrated that: (a) Infusions of epinephrine, norepinephrine, and phenylephrine in 5 per cent glucose for 7 to 10 hours have little effect on, or decrease, urinary aldosterone excretion. (b) Angiotensin II infusions markedly decrease sodium excretion and the Na/K ratio and increase the excretion of aldosterone; of its ring-A reduced metabolite, pregnane-3-α,18,21-triol,11,20-dione; and, to a much lesser degree, of cortisol and tetrahydrocortisone in all normal subjects studied. (c) In patients with benign essential hypertension, infusions of angiotensin also stimulate urinary aldosterone excretion hut have a completely opposite effect on electrolytes-that of increasing sodium output and the Na/K ratio. This basic difference in response to angiotensin points to a fundamental problem to be solved for a better understanding of the disease. It is felt that the relative or absolute excess of aldosterone over progesterone secretion may be the important adrenal disturbance among the basic factors involved in the pathogenesis of arterial hypertension. This disturbance is definitely linked with angiotensin and sodium regulation.