Abstract

The discovery in 1953 by the Taits and colleagues of the electrolyte active hormone aldosterone was a major landmark in the understanding of sodium homeostasis (1). Soon after, Bartter, Mills, Biglieri and Delea showed an influence of blood volume change on rate of aldosterone secretion (2). Laragh and Stoerk found increase of K intake increased aldosterone secretion (3). Several groups of investigators demonstrated that the anterior pituitary had an important but restricted role in the control of secretion in different species. The successful implementation of the idea of autotransplanting the left adrenal gland with attached renal vessels to a combined carotid artery-jugular vein skin loop in the neck of the Merino sheep, giving free access to artery and venous drainage in the conscious animal (4,5), was followed by demonstration that physiological decrease in plasma [Na] or increase in [K] acted directly on the adrenal to stimulate aldosterone secretion (6,7). The small rate of blood flow through the adrenal made it possible to produce locally in adrenal blood a wide range of change in composition with negligible systemic effect of the infusion. Thus it was possible formally to define precisely those factors which acted directly on the adrenal and those factors which, though influential on adrenal secretion, acted via an intermediate vector.KeywordsRenal DenervationAldosterone SecretionSalt AppetiteAldosterone ResponseConscious SheepThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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