Effect of Sodium Concentration on Aldosterone Secretion by Isolated Perfused Canine Adrenal Glands*

Abstract

Small changes in [Na] are not generally considered to have a major direct effect on aldosterone secretion. However a marked disruption in the renin-aldosterone relationship was observed in a variety of hypernatremic and hyponatremic states. Therefore, the hypothesis that small changes in [Na] have a potent direct effect on angiotensin II- and K-stimulated aldosterone secretion. The left adrenal gland, abdominal aorta and surrounding periadrenal tissue were surgically isolated from mongrel dogs and perfused with Ringers bicarbonate solution at a pressure of .apprx. 57 mm Hg. Infusion of a KCl test solution at the beginning and end of most experiments produced similar increases in aldosterone secretion, thus documenting the stability of these preparations. After a stable response was established to either a low dose of angiotensin II or a small increased in perfusate [K], the [Na] was changed by adding or removing NaCl. Changing perfusate [Na] from 152 to 139 mM during the infusion of either angioteins II or K caused 20- to 25-fold increases in aldosterone secretion. Increasing perfusate [Na] from 145 to 152 mM inhibited aldosterone secretion to a greater extent during stimulation by lower doses (40-50 pg/ml) than by higher doses (80-100 pg/ml) of angiotensin II. During moderate stimulation by angiotesin II or K, small changes in [Na] have a powerful inverse effect on aldosterone secretion by a direct action on the canine adrenal gland.