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

EDWARD G. SCHNEIDER, ROBERT E. TAYLOR, JR., KAREN J. RADKE and PHILLIP G. DAVIS

Department of Physiology and Biophysics, University of Tennessee Center for the Health Sciences Memphis, Tennessee 38163

Address requests for reprints to: Dr. Edward G. Schneider, Department of Physiology and Biophysics, The University of Tennessee Center for the Health Sciences, 894 Union Avenue, Memphis,Tennessee 38163.

Abstract

Small changes in sodium concentration ([Na]) are not generally considered to have a major direct effect on aldosterone secretion. However, a marked disruption in the renin-aldosterone relationship has been observed in a variety of hypernatremic and hyponatremic states. Therefore, we evaluated the hypothesis that small changes in [Na] have a potent direct effect on angiotensin II- and potassium-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 approximately 57 mm Hg. Infusion of a KC1 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 increase 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 angiotensin II or potassium 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. These data demonstrate that during moderate stimulation by angiotensin II or potassium, small changes in [Na] have a powerful inverse effect on aldosterone secretion by a direct action on the canine adrenal gland. (Endocrinology 115: 2195–2204, 1984)

Footnotes

^* This work was supported in part by USPHS Grant HL-27749.

Recipient of a summer research fellowship from the NIH (Grant T35-AM-07405.

Received January 12, 1984.

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