PLASMA DIGOXIN IMMUNOREACTIVITY AND ARTERIAL POTASSIUM RELAXATION AFTER QUINAPRIL THERAPY IN HYPERTENSIVE RATS

Plasma digitalis-like substance and altered function of arterial Na+,K +-ATPase have both been linked with elevated blood pressure, but the i nfluence of antihypertensive therapy on these factors remains unknown. Therefore, we treated spontaneously hypertensive rats and normotensiv e Wistar-Kyoto rats with the angiotensin-converting enzyme inhibitor q uinapril for 10 weeks. The therapy markedly reduced blood pressure and plasma digoxin immunoreactivity, and it normalized the elevated plasm a Na+:K+ ratio in the hypertensive animals. Relaxations of endothelium -denuded denervated arterial rings induced by return of potassium to t he organ bath upon precontractions elicited by potassium-free solution were used to evaluate the function of vascular Na+,K+-ATPase. The rat e of potassium relaxation was faster in quinapril-treated hypertensive rats and in both Wistar-Kyoto groups than in the hypertensive control s. Potassium relaxation was also effectively inhibited by the Na+,K+-A TPase inhibitor ouabain in all groups. In addition, arterial contracti ons to potassium chloride and relaxations to nitroprusside were examin ed. The contractions to lower concentrations of potassium chloride (20 mM) were enhanced in untreated hypertensive rats when compared with t he other groups, although the maximal responses were corresponding in all groups. The time to reach base-line tension after washout of potas sium chloride (125 mM) and the relaxations to nitroprusside did not di ffer in the study groups. In conclusion, the present results showed th at long-term angiotensin-converting enzyme inhibition in parallel redu ced plasma digoxin-like factor, enhanced arterial potassium relaxation (probably reflecting enhanced function of Na+,K+-ATPase) and normaliz ed plasma Na+:K+ ratio in this type of genetic hypertension.