ANGIOTENSIN, ELECTROLYTES AND ALDOSTERONE

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Abstract
Summary: The first part of this paper is concerned with some aspects of renal and endocrine effects on blood pressure and the moderation of these processes by the state of sodium balance. The effects of renin and angiotensin on aldosterone secretion and mechanisms involved in the appetite for salt are considered. The proposition is advanced that any role of aldosterone in the hypertensive process is likely to be understood only when the normal mechanism of control of aldosterone secretion is determined. It has been established by experiments on the transplanted adrenal of the sheep that ionic changes in arterial blood (decrease of sodium and increase of potassium concentration) act directly on the adrenal to stimulate aldosterone secretion, and that this is one pathway of physiological stimulation. This finding has been confirmed by experiments on the dog. The direct ionic effect on the adrenal is, however, probably not the major pathway of stimulation of aldosterone secretion. At present, a central unresolved question in this field of physiology is whether the renin angiotensin system is the normal pathway of stimulation of aldosterone secretion in sodium deficiency, or whether it is a mechanism which operates only in pathological states with renal damage such as malignant hypertension. Evidence such as the correlation between the histology of the juxtaglomerular region of the kidney and sodium balance is suggestive that renin has a physiological role. Consideration of the evidence derived from acute experiments on the effect of nephrectomy on aldosterone secretion indicates the necessity of further investigation on conscious animals under conditions which are as near normal as feasible