EFFECT OF VASOPRESSIN ON THE ACTIVITY OF THE Na⁺-K⁺ PUMP IN VASCULAR SMOOTH MUSCLE CELLS

Abstract

Plasma ADH levels are elevated in one-kidney, DOCA, salt and reduced renal mass hypertensive rats. Because ADH causes vasoconstriction and is involved in body fluid volume regulation, elevated plasma levels may play a role in the pathophysiology of hypertension. Also, ouabain-sensitive (OS) ⁸⁶Rb uptake, a measure of Na⁺-K⁺ pump activity, is decreased in rats with these models of hypertension. The effect of ADH on vascular Na⁺-K⁺ pump activity has never been studied. The purpose of the present study was to determine the effect of ADH on vascular Na⁺-K⁺ pump activity. The objectives were to 1) determine the effect of ADH (5 X 10⁻² Wm].) on OS and ouabain-insensitive (0I) ⁸⁶Rb uptake in rat rat tail arteries, 2) generate dose response curves to ADH for in vitro blood vessels, 3) determine the effect of contracting (10⁻² U/ml), moderately contracting (10⁻³ U/ml) and non-contracting (10⁻⁴ U/ml) doses of ADH on OS and OI ⁸⁶Rb uptake, and 4) use a vascular ADH antagonist to determine if these doses of ADH directly effect ⁸⁶Rb uptake in vascular smooth muscle cells. Compared to untreated vessels, OS and OI uptakes in vessels treated with 10⁻² U/ml and 5 X 10⁻² U/ml ADH were significantly decreased. ADH (10⁻⁴ U/ml) had no effect on blood vessel tension, 10⁻³ U/ml caused a moderate increase and 10⁻² U/ml produced a maximum increase in tension. In the presence of a vascular ADH antagonist no significant differences in OS or OI ⁸⁶Rb uptake were detected in ADH treated and untreated vessels. These findings suggest that the effect of maximally contracting doses of ADH on OS and OI 86Rb uptakes are probably secondary to vasoconstriction and the suppressed pump activity observed in certain low renin volume dependent models of hypertension cannot be attributed to altered ADH levels.