THE ROLE OF THE RENIN-ANGIOTENSIN SYSTEM IN THE CONTROL OF ALDOSTERONE SECRETION*

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Abstract
Crude saline extracts of dog kidney were fractionated by heat, dialysis, and ammonium sul-fate precipitation for aldosterone-stimulating and pressor activity. The 1.7 and 2.5 [image] (NH)2SO4 fractions, which are known to precipitate renin, were the only fractions with appreciable steroidogenic activity and only the 1.7 M fraction gave a statistically significant increase in aldosterone secretion. Pressor activity was closely associated with aldosterone-stimulating activity. Heating to 80[degree] C for 10 minutes destroyed all aldosterone-stimulating and pressor activity. The data provide strong suggestive evidence that the active agent in crude kidney extracts is renin. Extraction and assay of kidney tissue for renin showed a sevenfold greater renin content of kidneys from dogs with thoracic caval constriction than from normal dog kidneys. The response in arterial pressure to an intravenous injection of synthetic angiotensin II was markedly reduced in dogs with thoracic caval constriction and in Na-depleted dogs in comparison with the effect in normal dogs. The renal juxtaglomerular cells were hypergranulated and hyperplastic in dogs with thoracic caval constriction. Suprarenal aortic constriction of hypophysectomized dogs resulted in a 100% increase in aldosterone secretion and a 150% increase in corticosterone production. The steroidogenic response was associated with a drop in renal arterial pressure and renal blood flow, but renal vascular resistance increased. The findings in the present study support the view that the stimulus associated with a decrease in arterial pressure and blood flow in the kidney leads to secretion of renin by the juxtaglomerular cells. Renin via the formation of angiotensin II and the direct action of angiotensin II on the zona glomerulosa augments aldosterone secretion.