Journal of Clinical Endocrinology & Metabolism, Vol 41, 153-159, Copyright © 1975 by Endocrine Society

ARTICLES

Potassim-aldosterone-renin interrelationships

T Himathongkam, RG Dluhy and GH Williams

The present study was performed to assess the sensitivity of the renin- angiotensin-aldosterone axis to small changes in plasma potassium concentration within the physiologic range. Small increments in potassium levels were accomplished by graded constant infusions of potassium chloride over 2 h (0.17 meq/min; 0.33 meq/min; 0.5 meq/min) in 8 normal subjects on a 10 meq sodium-100 mgq potassium intake. Plasma levels of aldosterone, renin activity, angiotensin II, cortisol, potassium and sodium were measured at frequent intervals. There were no significant changes observed in plasma sodium, renin activity or angiotensin II levels while cortisol levels declined in the expected diurnal pattern. During the 0.17 meq/min (10 meq/h) infusion potassium levels did not increase significantly until 120 min while plasma aldosterone levels rose significantly at 30-60 min. The mean increment above control during the lowest infusion rate was 0.2 meq/liter (5%) for plasma potassium and 13 ng/100 ml (46%) for plasma aldostreone. Although there was a stepwise increase in the increments above control of both potassium and aldosterone levels as the rate of the infusion was increased, the most sensitive area of the dose response curve appears to be 0.1-0.5 meq/liter. in six normal subjects the potassium- lowering effect of glucose ingestion (0.25 g/kg/15 min over a 2-h period) was assessed. The mean maximal potassium decrement below control 0.3 meq/liter (8%) at 90 min was coincident with the mean plasma aldosterone decrement below control of 11 ng/100 ml (46%). Plasma aldosterone then rose to peak levels at 180 min (mean increment 22 ng/100 ml above nadir) while potassium levels remained below control. The rise in plasma aldosterone was associated with a parallel but more rapid rise in plasma renin activity, peaking at a level 108% above control. Ninety minutes after the termination of the glucose ingestion, plasma aldosterone returned to control levels but now in the setting of reduced levels of plasma potassium and elevated levels of plasma renin activity. The data support an important role for physiologic changes in extracellular potassium concentration in the control of aldosterone secretion and indicate that interpretation of studies assessing acute changes in plasma aldosterone must carefully consider minor simultaneous changes in plasma potassium levels. The data also document that acute changes in extracellular potassium concentration play a role in the regulation of renin secretion.

This article has been cited by other articles:

				T. S. Perlstein, M. Gerhard-Herman, N. K. Hollenberg, G. H. Williams, and A. Thomas Insulin Induces Renal Vasodilation, Increases Plasma Renin Activity, and Sensitizes the Renal Vasculature to Angiotensin Receptor Blockade in Healthy Subjects J. Am. Soc. Nephrol., March 1, 2007; 18(3): 944 - 951. [Abstract] [Full Text] [PDF]

				M. P. Ponda and T. H. Hostetter Aldosterone Antagonism in Chronic Kidney Disease Clin. J. Am. Soc. Nephrol., July 1, 2006; 1(4): 668 - 677. [Full Text] [PDF]

				A. SPAT and L. HUNYADY Control of Aldosterone Secretion: A Model for Convergence in Cellular Signaling Pathways Physiol Rev, April 1, 2004; 84(2): 489 - 539. [Abstract] [Full Text] [PDF]

				E. J. Lichtarowicz-Krynska, T. J. Cole, C. Camacho-H""bner, J. Britto, M. Levin, N. Klein, and A. Aynsley-Green Circulating Aldosterone Levels Are Unexpectedly Low in Children with Acute Meningococcal Disease J. Clin. Endocrinol. Metab., March 1, 2004; 89(3): 1410 - 1414. [Abstract] [Full Text] [PDF]

				J. K. Makara, P. Koncz, G. L. Petheo, and A. Spat Role of Cell Volume in K+-Induced Ca2+ Signaling by Rat Adrenal Glomerulosa Cells Endocrinology, November 1, 2003; 144(11): 4916 - 4922. [Abstract] [Full Text] [PDF]

				A. Kjar, U. Knigge, H. Jorgensen, and J. Warberg Dehydration-induced vasopressin secretion in humans: involvement of the histaminergic system Am J Physiol Endocrinol Metab, December 1, 2000; 279(6): E1305 - E1310. [Abstract] [Full Text] [PDF]

				W. R. Litchfield, C. Coolidge, P. Silva, R. P. Lifton, F. Fallo, G. H. Williams, and R. G. Dluhy Impaired Potassium-Stimulated Aldosterone Production: A Possible Explanation for Normokalemic Glucocorticoid-Remediable Aldosteronism J. Clin. Endocrinol. Metab., May 1, 1997; 82(5): 1507 - 1510. [Abstract] [Full Text] [PDF]