Published Online
on February 16, 2004

A more recent version of this article appeared on April 1, 2004

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Submitted on September 19, 2003
Revised on November 21, 2003

Urinary Potassium Excretion and Sodium Sensitivity in Blacks

Abraham Aviv^*; Norman K. Hollenberg; and Alan Weder

From the Hypertension Research Center (A.A.), Cardiovascular Research Institute University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark; Departments of Medicine and Radiology (N.K.H.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass; and Division of Hypertension (A.W.), Department of Internal Medicine, University of Michigan, Ann Arbor.

^* To whom correspondence should be addressed. E-mail: avivab{at}umdnj.edu.

Abstract--Based on racial differences in urinary potassium excretion and responses to diuretics, we present a model suggesting that a major cause of sodium sensitivity in blacks is an augmented activity of the Na-K-2Cl cotransport in the thick ascending limb of Henle’s loop. This would result in an increased ability to conserve not only sodium but also water, and an upward and rightward shift in the operating point of tubuloglomerular feedback, which may cause an increase in the glomerular capillary hydraulic pressure and predilection to glomerular injury with and without hypertension. In this sense, the biological implication of sodium sensitivity in blacks and in humans in general has ramifications above and beyond salt-evoked increase in blood pressure.

Key words: blacks • hypertension, essential • kidney • potassium • sodium

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