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Sodium pump activity in arteries of rats with Goldblatt hypertension
Abstract:
Several laboratories have reported evidence suggesting abnormalities in the activity of the sarcolemmal sodium pump in vascular smooth muscle in hypertension. The present experiments were designed to investigate the relationship of such changes to the status of the renin-angiotensin-aldosterone system and body fluid volumes. We assessed sodium pump activity in vitro in sodium-loaded tail artery and thoracic aorta freshly excised from rats with chronic one-kidney, one clip, and two-kidney, one clip hypertension, and from appropriate normotensive control rats. 86Rb uptake in the absence (total uptake) and presence of 1.0 mM ouabain (ouabain-insensitive uptake) was measured, and ouabain-sensitive uptake (nmole/mg dry weight/18 min) was calculated. There were increases in plasma renin activity in the two-kidney, one clip rats only. In the hypertensive rats there were significant increases (up to +60%) in the ouabain-sensitive and total 86Rb uptakes in both tail artery and aorta. The magnitude of increases in arterial tissue uptakes in the two forms of Goldblatt hypertension, and in one-kidney, one clip hypertensive rats given 0.9% saline to drink for 2 to 3 days before sacrifice, were similar. Further sodium loading of aortas from normotensive control rats did not increase their uptake. The results of this study provide no evidence for decreases in sodium pump activity, instead indicating that there are increases in the activity of the pump in the sarcolemma or arterial smooth muscle studied in vitro. These increases in pump activity do not appear to be related to altered activity of the renin-angiotensin-aldosterone system, to changes in body fluid volumes, or to increases in intracellular concentrations of sodium. Increases in numbers or concentration of sarcolemmal pump molecules or in their turnover rate may be involved. However, in vitro 86Rb uptake by tail artery and aorta may not reflect the status of sodium pump activity in resistance vessels in vivo.