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Hypertension, Vol 7, 277-286, Copyright © 1985 by American Heart Association
C Aalkjaer, K Kjeldsen, A Norgaard, T Clausen and MJ Mulvany
The possible role of Na+ in the development of hypertension in rats was
explored in measurements of intracellular Na+, 22Na efflux, and 3H- ouabain
binding sites in resistance vessels and skeletal muscles. In resistance
vessels obtained from 13-week-old spontaneously hypertensive rats (SHR) or
age-matched Wistar-Kyoto rats (WKY), (Na)i, total or ouabain-resistant 22Na
efflux, and the concentration of 3H-ouabain binding sites showed no
significant differences. Soleus muscles obtained from 6-week-old and
13-week-old SHR contained 5 to 11% more 3H- ouabain binding sites than
those of WKY. The small difference in ouabain binding probably was related
more to variations in growth rate and strain than to the hypertension. In
SHR and WKY the Na+ and K+ contents of gastrocnemius muscles were almost
identical at 6 and 13 weeks of age. By contrast, in Wistar rats in which
the (Na)i of skeletal muscle was increased sixfold by K+ depletion, the
systolic blood pressure was decreased by 10%. The K+ depletion was
associated with a 35 to 55% decrease in the concentration of 3H-ouabain
binding sites in both resistance vessels and skeletal muscles. The results
provide no support for any simple cause-effect relationships between either
elevated (Na)i or altered concentration of 3H-ouabain binding sites and
hypertension in SHR.
ARTICLES
Ouabain binding and Na+ content in resistance vessels and skeletal muscles of spontaneously hypertensive rats and K+-depleted rats
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