Endothelium-derived relaxing factor (nitric oxide) has a tonic vasodilating action on coronary collateral vessels

Objectives. We sought to determine whether endothelium-derived relaxing factor (nitrix oxide) exerts a tonic vasodilating effect on coronary collateral channels developed in response to myocardial ischemia.Background. Although the coronary collateral circulation is known to react to several vasoactive agents, the role of endogenously produced nitric oxide is unclear.Methods. Coronary collateral channels were induced in the left circumflex artery bed of 12 chronically instrumented dogs by either ameroid implantation or repeated occlusion of the left circumflex coronary artery. With the native circumflex artery occluded, aortic and circumflex pressures and microsphere flows were measured before and after systemic administration of N^G-nitro-l-arginine methyl ester, an arginine analogue known to block the synthesis of nitric oxide.Results. N^G-nitro-l-arginine methyl ester increased mean aortic pressure from a mean ± SEM of 92 ± 4 to 114 ± 4 mm Hg, whereas pressure in the occluded circumflex artery decreased from 61 ± 4 to 55 ± 4 mm Hg. The increase in aortic-circumflex pressure gradient (from 31 ± 4 to 59 ± 5 mm Hg) was accompanied by a decrease in flow in the circumflex bed (from 1.31 ± 0.14 to 1.09 ± 0.15 ml/min per g), resulting in an increase in coronary collateral resistance averaging 173 ± 37% (from 26 ± 4 to 64 ± 9 mm Hg/ml per min per g, p < 0.01). The increase in collateral resistance could be partially reversed by administration of l-arginine.Conclusions. We conclude that nitric oxide normally exerts a substantial tonic dilating effect in coronary collateral vessels. Disease-induced alterations in endothelial function may limit collateral perfusion importantly.