Abstract
Abstract
To chronically decrease activity of the ouabain-sensitive sodium pump in vascular smooth muscle, we administered digoxin (60 μg/kg, followed by 8-16 μg/kg/12 hr, iv) to five male mongrel dogs for 4 weeks. Serum digoxin levels were monitored and maintained at concentrations sufficient to continuously inhibit the sodium pump. Blood pressures and serum Na+ and K+ concentrations of the treated dogs did not change significantly. Five paired control dogs received saline injections. Two hours after a final injection, samples of small mesenteric arteries and veins were obtained under sodium pentobarbital (30 mg/kg, iv) anesthesia for measurement of vessel wall 86Rb uptake and water content. In veins there were no significant changes in pump activity or water content. In contrast, in arteries the ouabain-sensitive 86Rb uptake was depressed (P < 0.02) in treated dogs. Accompanying this depression was an increase, averaging 6.2% (P < 0.05), in mesenteric artery wall water content. These data provide evidence associating chronic digitalis suppression of the sodium pump in arteries with the development of wall edema. These results are compatible with the hypothesis that inhibition of the sarcolemmal sodium pump of arteries may underlie the “waterlogging” of these vessels in hypertension.
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