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. 1990 Oct 13;336(8720):897-900.
doi: 10.1016/0140-6736(90)92269-n.

Low basal and stimulated release of nitric oxide in atherosclerotic epicardial coronary arteries

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Low basal and stimulated release of nitric oxide in atherosclerotic epicardial coronary arteries

A H Chester et al. Lancet. .

Abstract

Endothelium-dependent relaxations in response to substance P and bradykinin were lower in atherosclerotic than in normal human coronary arteries. The relaxation induced by substance P was inhibited by L-NG-monomethylarginine (L-NMMA), which shows that release of nitric oxide is involved in the mediation of endothelium-dependent relaxation in these arteries. L-NMMA also inhibited a basal component of endothelium-dependent relaxation. The basal secretion of nitric oxide was significantly lower in diseased than in normal arteries. These findings suggest that atherosclerotic human coronary arteries lack an important protective mechanism that normally guards against vasospasm and thrombosis.

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  • Endothelial dysfunction in vascular disease.
    Dinh-Xuan AT, Pepke-Zaba J, Cremona G, Butt AY, Higenbottam TW. Dinh-Xuan AT, et al. Lancet. 1990 Nov 17;336(8725):1253. doi: 10.1016/0140-6736(90)92869-j. Lancet. 1990. PMID: 1978093 No abstract available.

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