Endocrinology, Vol 116, 1621-1626, Copyright © 1985 by Endocrine Society

ARTICLES

Effect of osmolality on aldosterone secretion

EG Schneider, KJ Radke, DA Ulderich and RE Taylor Jr

The purpose of these experiments was to determine if the powerful effect of sodium chloride concentration on angiotensin II- and potassium-stimulated aldosterone secretion by isolated perfused adrenal glands is mediated by the sodium or chloride ion or by the obligatory change in osmolality. We used isolated Ringer's bicarbonate perfused canine adrenal gland preparations to determine the effects of a variety of isosmotic, hyperosmotic, and hyposmotic solutions on angiotensin II- and potassium-stimulated aldosterone secretion. When we increased the osmolality of the perfusion medium (8-10 mosmol) by the addition of NaCl, sucrose, mannitol, or glucose, angiotensin II-stimulated aldosterone secretion was inhibited to a similar extent, whereas urea addition had no effect. Similarly, when we increased the osmolality of the perfusion medium (8-10 mosmol) by the addition of NaCl, sucrose, or mannitol, potassium-stimulated aldosterone secretion was also inhibited to a similar extent. In contrast to the increase in angiotensin II- and potassium-stimulated aldosterone secretion observed during hyposmotic reductions in NaCl concentration, (addition of sucrose) did not increase angiotensin II- or potassium-stimulated aldosterone secretion. Even the marked increase in aldosterone secretion caused by large hyposmotic reduction in NaCl concentration did not occur with an equivalent isosmotic reduction in NaCl concentration. These results clearly demonstrate that changes in NaCl concentration affect aldosterone secretion by a mechanism sensitive to the osmolality. Moreover, since hyperosmolality caused by urea addition had no effect on angiotensin II-stimulated aldosterone secretion, changes in intracellular volume or composition appear to be an important modulator of aldosterone secretion.

This article has been cited by other articles:

				D. G. Romero, M. W. Plonczynski, B. L. Welsh, C. E. Gomez-Sanchez, M. Y. Zhou, and E. P. Gomez-Sanchez Gene expression profile in rat adrenal zona glomerulosa cells stimulated with aldosterone secretagogues Physiol Genomics, December 19, 2007; 32(1): 117 - 127. [Abstract] [Full Text] [PDF]

				S. Tiwari, R. K. Packer, X. Hu, Y. Sugimura, J. G. Verbalis, and C. A. Ecelbarger Increased renal {alpha}-ENaC and NCC abundance and elevated blood pressure are independent of hyperaldosteronism in vasopressin escape Am J Physiol Renal Physiol, July 1, 2006; 291(1): F49 - F57. [Abstract] [Full Text] [PDF]

				J. Song, X. Hu, O. Khan, Y. Tian, J. G. Verbalis, and C. A. Ecelbarger Increased blood pressure, aldosterone activity, and regional differences in renal ENaC protein during vasopressin escape Am J Physiol Renal Physiol, November 1, 2004; 287(5): F1076 - F1083. [Abstract] [Full Text] [PDF]

				J. K. Makara, G. L. Petheo, A. Toth, and A. Spat Effect of Osmolarity on Aldosterone Production by Rat Adrenal Glomerulosa Cells Endocrinology, May 1, 2000; 141(5): 1705 - 1710. [Abstract] [Full Text] [PDF]

				F. LANG, G. L. BUSCH, M. RITTER, H. VOLKL, S. WALDEGGER, E. GULBINS, and D. HAUSSINGER Functional Significance of Cell Volume Regulatory Mechanisms Physiol Rev, January 1, 1998; 78(1): 247 - 306. [Abstract] [Full Text] [PDF]