RENAL ORIGIN OF AN ALDOSTERONE-STIMULATING HORMONE IN DOGS WITH THORACIC CAVAL CONSTRICTION AND IN SODIUM-DEPLETED DOGS

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Abstract
The effects of nephrectomy on aldosterone and corticosterone secretion have been studied in 16 dogs with chronic thoracic caval constriction and in 8 chronic Na-depleted animals. In the preliminary study with the anterior pituitary intact, aldosterone secretion failed to decrease consistently after nephrectomy, apparently because of the high circulating level of ACTH. Consequently, for the definitive study, hypophysectomy was performed before nephrectomy. In the hypophysectomized dogs with thoracic caval constriction, nephrectomy resulted in a fall in aldosterone secretion in every animal from an average control value of 0.033 to 0006 [mu]g per minute, an 82% fall, and corticosterone output decreased from a very low rate of secretion of 0.20 to 0.04 [mu]g/minute, an 80% fall. A similar striking drop in both aldosterone and corticosterone secretion followed nephrectomy in the Na-depleted hypophysectomized dogs. The high initial control values for aldosterone secretion before nephrectomy of both hypophysectomized caval and hypophysectomized Na-depleted dogs demonstrated hypersecretion of aldosterone in the absence of the anterior pituitary. The findings provide evidence for increased secretion of an aldosterone-stimulating hormone by the kidney in response to chronic thoracic caval constriction and to chronic Na depletion.