Evidence for enhanced sodium transport in the tail artery of the spontaneously hypertensive rat.

Transmembrane Na+ and K+ gradients in the rat tail artery were dissipated by overnight incubation in K-free PSS at 10 degrees C and then allowed to recover in normal physiologic salt solution (PSS) at 37 degrees 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 degrees C, or in the presence of 1 mM ouabain at both 3 degrees C and 37 degrees C. Active exchange was switched on by an abrupt transfer of the tissue from 3 degrees C to 37 degrees C. Active exchange, measured in perfused, superfused, or sequentially incubated arteries, was distinctly enhanced in young (16-, 20- and 26-week-old) spontaneously hypertensive rats (SHR) of the Okamoto strain compared with age-matched Wistar-Kyoto normotensive (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 Nai and Ki were measured after washing the tissues for 45 minutes at 3 degrees 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 Na0 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 degrees C.