[Modification of phenylephrine induced contraction of human vessel rings by L-arginine and L-arginine methyl ester].

BACKGROUND

Endothelial dysfunction is associated to a lower production of nitric oxide and a reduction of endothelium mediated vasodilation.

AIM

To study the effects of pharmacological agents that modify nitric oxide synthetase (NOS) activity on tension changes induced by phenylephrine in rings of internal mammary and radial arteries and saphenous vein.

MATERIAL AND METHODS

Vessel rings of 7 to 10 mm length were obtained from 32 patients subjected to coronary vascular surgery Fourteen samples of radial artery, 12 samples of internal mammary artery and 15 samples of saphenous vein were obtained. A maximal contraction was induced with KC1 and dose response curves for phenylephrine (FE) in the absence or presence of L-arginine and L-arginine methyl ester (L-NAME), were constructed.

RESULTS

The tension induced by FE in internal mammary artery and saphenous vein reached a maximum, near 90% of 80 mM KCl-induced contraction, but in the radial artery, it reached a maximum of 63% (p <0.05). In all vessels, the dose response curves were significantly shifted to the right by L-arginine and to the left by L-NAME.

CONCLUSIONS

Pre-incubation of human rings with L-ARG or L-NAME, changed the response to FE induced contraction, which may be related to different degrees of endothelial nitric oxide production or NO sensitivity. The basal NO production in radial artery seems to be larger than the other vessels.