Effect of different vasodilators on NTPDase activity in healthy and hypertensive patients

Abstract

Introduction The thrombogenic process that affects the hypertensive patient is associated with regulatory mechanisms present in the vascular endothelium. These mechanisms involve release of an endothelium-derived relaxing factor, ectonucleotidase activity and calcium ion concentration. Methods Interference with ENTPDase activity in platelets of hypertensive patients and healthy donors was evaluated for arginine, sodium nitroprusside, and hydralazine. In addition, the kinetic behavior of NTPDase was determined in the presence of the vasodilator that showed the greatest inhibitory influence. Results Vasodilators decreased NTPDase activity with ATP and ADP as substrates. In controls, hydrolysis was increased in the presence of arginine. Captopril did not affect enzyme activities. The dose response for increasing sodium nitroprusside was biphasic. Kinetic behavior studies were estimated in the presence of sodium nitroprusside, which caused a mixed inhibition. The K m values increased and V max decreased with increasing sodium nitroprusside concentrations. The IC 50 and K i values indicated that the vasodilator was a strong NTPDase inhibitor when tested for the control and hypertensive group, using ATP and ADP as substrate, respectively. Conclusion It is postulated that there was an interaction between vasodilators, NO donors and inhibition of NTPDase.