title: Attenuation of acetylcholine-induced vasoconstriction by L-arginine is related to the progression of atherosclerosis.
abstract: To determine if L-arginine, a precursor of the endothelium-derived relaxing factor, restores endothelium-dependent dilation in human coronary arteries, we studied 21 patients in whom the lumina of the coronary arteries were angiographically smooth or slightly irregular and in whom there was a constrictor response to acetylcholine (ACh) in the left anterior descending coronary artery or the circumflex coronary artery. We examined the response to intracoronary ACh before and after infusion of L-arginine by measuring coronary diameter with quantitative angiography. Intracoronary injection of ACh produced vasoconstriction in the majority of patients with coronary risk factors. The percentage diameter change in smooth segments in patients with entirely smooth coronary arteries (group 1, n = 44) from baseline was -20.7% +/- 17.4%. During systemic infusion of L-arginine, the constrictor response to ACh in these segments was significantly attenuated (-2.2% +/- 15.1% from baseline, p < 0.01, ACh alone vs ACh during L-arginine infusion). In smooth segments in patients with luminal irregularities in the other coronary arteries (group 2, n = 19), ACh produced a marked constriction (-32.5% +/- 22.5% from baseline, p < 0.05, group 1 vs group 2). Infusion of L-arginine also attenuated ACh-induced vasoconstriction in these segments (-9.7% +/- 14.1% from baseline, p < 0.01, ACh vs ACh during L-arginine infusion). In segments with irregular lumina (group 3, n = 26), ACh produced more prominent vasoconstriction. The percentage diameter change was -40.9% +/- 26.5% from baseline (p < 0.01 vs group 1).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Internal Medicine I, Osaka Medical College, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Otsuji
authors.forename: O
authors.initials: O
authors.lastname: Nakajima
authors.forename: S
authors.initials: S
authors.lastname: Waku
authors.forename: S
authors.initials: S
authors.lastname: Kojima
authors.forename: H
authors.initials: H
authors.lastname: Hosokawa
authors.forename: I
authors.initials: I
authors.lastname: Kinoshita
authors.forename: T
authors.initials: T
authors.lastname: Okubo
authors.forename: S
authors.initials: S
authors.lastname: Tamoto
authors.forename: K
authors.initials: K
authors.lastname: Takada
authors.forename: T
authors.initials: T
authors.lastname: Ishihara
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000328:Adult; D000368:Aged; D001120:Arginine / Q000008:administration & dosage / Q000494:pharmacology*; D001794:Blood Pressure; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects* / Q000473:pathology; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology; D005260:Female; D006339:Heart Rate; D006801:Humans; D007269:Injections, Intra-Arterial; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013237:Stereoisomerism; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation
chemical_list: D001120:Arginine; D000109:Acetylcholine