No abstract

No abstract

Within the last year, evidence (1-4) has accumulated to show that the kidney secretes a hormone which is a prime regulator of aldosterone secretion. The renal origin of an aldosteronestimulating hormone (ASH) has been demonstrated following acute blood loss (1-3), during chronic thoracic caval constriction (4), and during chronic Na depletion (4). Nephrectomizedhypophysectomized dogs failed to respond to acute hemorrhage with an increase in aldosterone secretion, and acute bilateral nephrectomy of hypophysectomized caval and hypophysectomized Nadepleted dogs resulted in a marked drop in aldosterone secretion. Furthermore, crude saline extracts of kidney produced a striking increase in aldosterone secretion (1-5). In malignant experimental renal hypertension, hyperaldosteronism was consistently present (6). These findings and the reports that renin preparations (6) and synthetic angiotensin II (6-8) increase the rate of aldosterone production suggest the possibility that ASH is renin.The present experiments were undertaken to determine the chemical nature of this ASH by fractionation of crude kidney extracts for aldosterone-stimulating and pressor activity. The renin content of kidneys from dogs with thoracic caval constriction and secondary hyperaldosteronism and from normal dogs has been compared.

No abstract