Hypertension, Vol 3, 306-312, Copyright © 1981 by American Heart Association
HW Overbeck, DD Ku and JP Rapp
Decreased activity of the electrogenic sodium pump of vascular smooth
muscle has been reported in several forms of experimental hypertension and
may play an important role in basic disease mechanisms. It has been
proposed that such pump suppression may characterize volume-expanded forms
of hypertension. The present investigation tested this latter hypothesis.
Sodium pump activity was assessed in vitro in sodium-loaded tail artery and
thoracic aorta freshly excised from Dahl salt-sensitive (S) and
salt-resistant (R) rats on low (0.4%) or high (8%) NaCl diets for 5 to 7
weeks. Rubidium (86Rb) uptake in the absence (total uptake) and presence
(ouabain-insensitive uptake) of 1.0mM ouabain was measured and
ouabain-sensitive uptake (nmole/mg dry weight/10 min) was calculated. In S
rats, salt feeding was accompanied by elevation of arterial pressure,
cardiac hypertrophy, increases of 20% to 30% in total blood volume, and
increases in the ouabain-sensitive, ouabain- insensitive, and total uptakes
in the aorta, but no significant change in uptakes in the tail artery.
However, ouabain-sensitive uptake in the tail artery of all S rats exceeded
than in R rats. There was no evidence of a decrease in vascular sodium pump
activity accompanying hypertension in either artery. Therefore, the results
of this study provide no evidence in support of the hypothesis that pump
suppression in vascular smooth muscle characterizes volume-expanded forms
of hypertension. It is unlikely that the observed increases in vascular
pump activity in S rats reflected intracellular sodium concentrations
higher than those in the control rats. Rather, increases in the numbers of
pump molecules or in their turnover rate are probably involved.
ARTICLES
Sodium pump activity in arteries of Dahl salt-sensitive rats
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