Regulation of femoral vascular resistance by adenine nucleotides via endothelial and smooth muscle receptors.

It is well established that adenosine (ADO) and adenine nucleotides are potent vasodilators, but their role in local blood flow control is still under debate. Recent findings on contribution of vascular endothelium to the vasomotor regulation pointed out this problem. In the present study the effects of adenine nucleotides were investigated in vivo on the femoral arterial flow (FAF) and femoral vascular resistance (FVR). Selective suppression of the endothelium mediated dilation was achieved by gossypol (35 mumol/l). On intact hindlimbs ADO (4 mmol/l) and ATP (0.5 mmol/l) elicited 3.5-fold increase of FAF, in average. Resistance decreased by 6.24 +/- 0.58 and 7.23 +/- 1.12 peripheral resistance units (PRU100), respectively. After gossypol, ATP-induced dilation was either significantly suppressed (resistance-decrease was 3.70 +/- 0.58 PRU100; p less than 0.02 vs control) or turned to strong constriction (FAF decreased by 50%). ADO-induced dilation remained unchanged. These results, in agreement with in vitro data, suggest that adenosine directly relaxes the vascular smooth muscle of resistance vessels via P1-purinoceptors, while ATP-induced vasomotion is composed of a dilator effect mediated by endothelial P2y-receptors, and a direct constrictor effect on the vascular smooth muscle via P2x-purinoceptors.