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J Am Coll Cardiol. 1996 May;27(6):1444-9.

Basal release of endothelium-derived nitric oxide at site of spasm in patients with variant angina.

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Research Institute of Angiocardiology and Cardiovascular Clinic, Faculty of Medicine, Kyushu University, Fukuoka, Japan.



The aim of this study was to investigate the basal release of nitric oxide at spastic sites in patients with variant angina.


We previously reported that endothelium-dependent dilator responses to acetylcholine, substance P and bradykinin are preserved at the site of coronary artery spasm. However, it is not known whether the basal release of endothelium-derived nitric oxide is altered at the spastic site.


The effects of intracoronary N(G)-monomethyl-L-arginine (L-NMMA, an inhibitor of nitric oxide synthesis) at cumulative doses of 50, 100 and 200 micromol on basal coronary artery tone were investigated in eight patients with variant angina and normal coronary angiograms and in eight control subjects. The lumen diameters of large epicardial coronary arteries were assessed by quantitative coronary arteriography.


Coronary spasm was provoked by the intracoronary administration of acetylcholine in all patients with variant angina. L-NMMA did not alter the arterial pressure and heart rate but significantly decreased the coronary artery diameter at spastic and nonspastic sites. Constrictive responses to L-NMMA were significantly greater (p < 0.01) at the spastic site (constriction by 200 micromol, 22+/-7%, mean +/- SD) than at the nonspastic site (10+/-7%). Constrictive responses to L-NMMA at the nonspastic site in patients with variant angina were comparable to those in the control subjects.


These findings support the hypothesis that the basal release of nitric oxide may not be decreased at the spastic site in patients with variant angina.

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