Function of the sodium pump in arterial smooth muscle in experimental hypertension: role of pressure.

Several laboratories have reported evidence suggesting that in hypertension there are abnormalities in the activity of the sarcolemmal sodium pump in vascular smooth muscle. In the present study, by sampling tissue from both hypertensive and normotensive portions of the arterial tree in coarctation hypertension, we investigated the relationship of such abnormalities to the elevated intravascular pressure. Additionally, we measured plasma renin activity and body fluid volumes. We assessed sodium pump activity in vitro in sodium-loaded arteries freshly excised from rats with chronic coarctation hypertension (abdominal aorta constricted above the renal arteries 4 to 5 weeks previously) and from normotensive sham-coarcted rats; these included the tail artery, the hypertensive thoracic aorta, and the normotensive portion of the abdominal aorta below the clip. The Rb uptake in the absence (total uptake) and presence (ouabain-insensitive uptake) of 1.0 mM ouabain was measured, and ouabain-sensitive uptake (nmole/mg dry weight/10 min) was calculated. In the rats with coarctation hypertension, there were significant increases in the ouabain-sensitive and total MRb uptakes in both the thoracic and abdominal aorta, but no abnormalities in Rb uptake in the tail artery. The higher uptakes in tissue from coarcted rats could not be attributed to increased levels of intracellular sodium. Plasma renin activity was elevated in the coarcted rats, but no changes in body fluid volumes were detected. This study provides evidence that increases in the activity of the sodium pump, similar to those we have observed in tissue from rats with salt-induced or Goldblatt hypertension, occur in conduit arteries of rats with coarctation hypertension studied in vitro. Because similar increases occur in vascular smooth muscle of the normotensive and hypertensive portions of the aorta, these pump abnormalities in arteries do not appear to be the direct result of increased intravascular pressure and probably are not attributable to tissue hyperplasia. (Hypertension 4: 394-399, 1982)