Sodium-potassium pump activity in reduced renal-mass hypertension.

We have previously reported that ouabain-sensitive "Rb uptake, a measure of Na-K pump activity, is decreased in blood vessels of animals with several low renin, and probably volumedependent models of hypertension likely due to the action of a circulating sodium transport inhibitor. In this paper we summarize a detailed study of these and other related parameters in a model known to be volume expanded, reduced renal-mass hypertension in rats. We measured cardiovascular muscle cell Na-K pump activity in control normotensive and experimental hypertensive reduced renalmass rats, assayed super nates of boiled plasma from these rats for presence of a circulating Na transport inhibitor and studied the effects of anteroventral third ventricle (AV3V) lesions and central sympathectomy (by intraventricular injection of 6-hydroxydopamine) on development of reduced renal-mass hypertension, and on vascular Na-K pump activity and level of circulating Na transport inhibitors). We also measured the effect of dietary sodium restriction on reduced renal-mass hypertension, cardiovascular muscle cell Na-K pump activity and level of the circulating Na transport inhibitor. Compared to the normotensive control rats, the experimental hypertensive rats had increased extracellular fluid volume, decreased plasma renin activity, increased level of a circulating Na transport inhibitor, decreased vascular Na-K pump activity (even after in vitro chemical sympathectomy) and decreased cardiac microsomal Na-K-ATPase activity. Pump suppression and development of hypertension were temporally associated. Both AV3V lesions and central sympathectomy prevented development of reduced renal-mass hypertension, inhibition of vascular Na-K pump activity, and appearance of a circulating Na transport inhibitor. Withdrawal of saline reversed reduced renal-mass hypertension as well as vascular pump suppression and increased levels of a circulating pump inhibitor. These data support the hypothesis that inhibition of cardiovascular muscle cell Na-K pump activity by a circulating Na transport inhibitor that is released from or influenced by the AV3V area of the brain plays an important role in the mechanism of some types of low renin experimental hypertension. (Hypertension 5 (supp I): I-94-I-100, 1983)