Alteration in the Sarcolemmal Na+-K+Pump of Hindquarters Resistance Arteries in Doca-Salt Rats

It has been suggested that a circulating inhibitor of the Na(+)-K+ pump contributes to the development and maintenance of DOCA-salt hypertension. However, the discordant results have been reported as to whether the sarcolemmal Na(+)-K+ pump in DOCA-salt hypertension is inhibited. Furthermore, no study has examined alteration in the sarcolemmal Na(+)-K+ pump of the true resistance arteries. We examined hindquarters vasoconstriction induced by ouabain (10(-3) M) in the vascularly isolated hindquarters of the DOCA-salt treated or control rats, which were perfused with Krebs-Henseleit solution. Hindquarters vasoconstriction induced by ouabain (10(-3) M) was greater in the prehypertensive and hypertensive DOCA-salt rats than in the corresponding control rats (p less than 0.01). We also examined hindquarters vasoconstriction induced by ouabain (10(-3) M) in the vascularly isolated hindquarters of the normal assay rats which were perfused by the plasma obtained from the DOCA-salt or control rats. The plasma of the prehypertensive and hypertensive DOCA-salt rats attenuated ouabain-induced hindquarters vasoconstriction in the assay rats (p less than 0.01). The plasma of the DOCA-salt rats did not alter nonspecific vasoconstriction caused by barium chloride. These results suggest that the plasma of the prehypertensive and hypertensive DOCA-salt rats had an inhibitor of the sarcolemmal Na(+)-K+ pump of the resistance arteries, but the sarcolemmal Na(+)-K+ pump molecules of the resistance arteries of those rats were increased. The in vivo activity of the sarcolemmal pump of the resistance arteries of the DOCA-salt rats would be determined by the relative influence of increased pump molecules and a circulating pump inhibitor.