Regulatory role of nitric oxide on the cardiac Na,K-ATPase in hypertension

Abstract

The present study was oriented to regulatory role of nitric oxide on functional properties of the cardiac Na,K-ATPase in three various animal models of hypertension: spontaneously hypertensive male rats (SHR) with increased activity of nitric oxide synthase (NOS) by 60% (Sh1), SHR with decreased activity of NOS by 40% (Sh2) and rats with hypertension induced by L-NAME (40mg/kg/day) with depressed activity of NOS by 72% (LN). Studying the utilization of energy substrate we observed higher Na,K-ATPase activity in the whole concentration range of ATP in Sh1 and decreased activity in Sh2 and LN. Evaluation of kinetic parameters revealed an increase of Vmax value by 37% in Sh1 and decrease by 30% in Sh2 and 17% in LN. The KM value remained unchanged in Sh2 and LN, but was higher by 38% in Sh1 indicating increased affinity of the ATP binding site, as compared to controls. During the activation with Na+ we observed increased Vmax by 64% and increased KNa by 106% in Sh1. In Sh2 we found decreased Vmax by 40% and increased KNa by 38%. In LN, the enzyme showed unchanged V max with increased KNa by 50%. The above data indicate a positive role of increased activity of NOS in improvement of utilization of ATP as well as enhanced binding of Na+ by the cardiac Na,K-ATPase.