Konkurrenz zwischen endothelabhängiger und Nitroglygerin-induzierter koronarer Vasodilatation [Competition between endothelium-dependent and nitroglycerin-induced coronary vasodilation].

UNLABELLED: Intact vascular endothelium can relax the smooth muscle by liberation of EDRF (endothelium-derived relaxing factor) and thus induce vasodilation. We investigated to what extent functional integrity of the endothelium modifies the dilatory capacity of coronary arteries and which influence nitroglycerin exerts on endothelium-dependent relaxation mechanism. In 74 coronary segments from eight patients with coronary artery disease, coronary artery diameters were measured before (C1) and 90 s after intracoronary infusion of the endothelium-dependent vasodilator bradykinin (0.1 mM) by means of a computer-assisted contour assessment system (CAAS). The same segments were then measured before (C2; 10 min after C1) and 90 s after an intracoronary infusion of the endothelium-independent vasodilator nitroglycerin (0.29 mM). By dividing diameter increases after bradykinin in group I less than 0.15 mm, n = 42 segments and group II: greater than 0.45 mm, n = 32 segments, the following diameters were obtained (mean +/- SD): (table; see text) CONCLUSION: In atherosclerotic coronary segments with impaired endothelium and consecutively reduced endothelium-dependent dilation the vasodilatory capacity of nitroglycerin is enhanced. Due to a competitive effect on the final common biochemical pathway, i.e., stimulation of soluble guanylate cyclase and elevation of intracellular levels of cyclic guanosylmonophosphate (cGMP) nitrovasodilators can facilitate insufficient endogenous relaxation of vascular smooth muscle.