Hypertension, Vol 11, 141-146, Copyright © 1988 by American Heart Association
JB Smith, MB Wade, NS Fineberg and MH Weinberger
Primary aldosteronism is an uncommon cause of hypertension but one of
particular interest because of its distinctive pathophysiological mechanism
of blood pressure elevation. Aldosterone has been associated with increased
Na+,K+-adenosine triphosphatase (ATPase) activity, but there is controversy
over which sodium transport parameters are responsible for this increase.
We measured intracellular sodium, ouabain-sensitive and ouabain-insensitive
sodium efflux, and the number of Na+,K+-ATPase sites of washed
erythrocytes, as well as Na+-Li+ countertransport and the Li+-K+
cotransport rate constant of lithium- loaded red blood cells (RBCs) in six
patients with primary aldosteronism and in 50 normal subjects.
Ouabain-sensitive sodium efflux was significantly (p less than 0.001)
higher for the primary aldosteronism patients than for normal subjects
(1.85 +/- 0.29 vs 1.51 +/- 0.21 mmol/L RBC/hr) even though the
intracellular sodium concentration (7.2 +/- 1.5 vs 6.7 +/- 1.9 mM) and the
number of the Na+,K+-ATPase sites per RBC (331 +/- 52 vs 385 +/- 97) were
not increased. The elevated sodium efflux appeared to be due to a
significant (p less than 0.001) increase in the rate constant (1.60 +/-
0.12 x 10(-15) vs 1.28 +/- 0.15 x 10(-15) mmol/site/hr) of the ouabain-
sensitive sodium efflux. The rate constant decreased significantly (p less
than 0.01) after treatment.
ARTICLES
Sodium transport parameters in erythrocytes of patients with primary aldosteronism
Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907.
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