EVIDENCE FOR ENHANCED SODIUM-TRANSPORT IN THE TAIL ARTERY OF THE SPONTANEOUSLY HYPERTENSIVE RAT

Transraembrane Na+and K+gradients in the rat tail artery were dissipated by overnight incubation in K-free PSS at 10°C and then allowed to recover in normal physiologic salt solution (PSS) at 37°C. The active extrusion of Na+and uptake of K+during the recovery period was monitored with Na+and K+selective glass electrodes. Passive exchanges were differentiated by re-admitting K+at 3°C, or in the presence of 1 mM ouabain at both 3°C and 37°C. Active exchange was switched on by an abrupt transfer of the tissue from 3°C to 37°C. Active exchange, measured in perfused, supervised, or sequentially incubated arteries, was distinctly enhanced in young (16-, 20- and 26-week-old) spontaneously hypertensive rats (SHR) qf the Okamoto strain compared with age-matched Wistar-Kyoto normotensire (WKY) controls. No such difference was observed in rats with hypertension of 7 or 12 weeks' duration and equal severity induced by unilateral constriction of the renal artery. Steady-state Na, and K, were measured after washing the tissues for 45 minutes at 3°C in lithium-substituted medium to exchange extracellular sodium with lithium. Cell sodium in these tissues was further partitioned into a free component proportional to [Nab and an independent, constrained component. Cell potassium was found to be distinctly elevated in 2- and 4-month-old SHR, while free cell sodium remained normal, despite increased cell permeability demonstrable in a significant exchange of lithium for cell potassium and sodium even at 3°C. © 1979 American Heart Association, Inc.