Aim: 

The aim of present study was the investigation of regulatory role of nitric oxide (NO) on functional properties of the cardiac Na⁺,K⁺-ATPase during hypertension.

Methods: 

The first group was represented by spontaneously hypertensive rats (SHR) with increased synthesis of NO (Sh1). The second group of SHR revealed decreased synthesis of NO (Sh2) and in the third group (LN), the hypertension was induced by administration of L-NAME (40mg/kg/day). The kinetics of Na⁺,K⁺-ATPase were estimated by measuring the splitting of ATP by 50 mg of sarcolemmal proteins in dependence of the substrate and the cofactor concentrations.

Results: 

Studying the utilization of energy substrate ATP we observed higher Na⁺,K⁺-ATPase activity for Sh1, and depressed activity in Sh2 and LN. Evaluation of kinetic parameters revealed increased V_max in Sh1 and decreased values in Sh2 and LN. The affinity of the ATP binding site was improved in Sh1 as indicated by the lowered K_m. In Sh2 and LN groups the K _m value remained unchanged. During the activation with Na⁺ the V _max and K values increased in the Sh1. The Sh2 revealed decreased V and increased K_Na. In LN the enzyme activity was depressed mainly at lower concentrations of NaCl, showing unchanged V_max with increased K_Na.

Conclusion: 

Our data indicate a positive role of increased NO-synthesis in improvement of utilization of ATP as well as enhanced Na⁺-binding by the cardiac Na⁺,K⁺-ATPase.

Supported by Slovak grant agencies: APVV – 51-059505, 2/7127/27