Nitric oxide-mediated vasodilatation is decreased in forearm resistance vessels in patients with coronary spastic angina

Citation
Y. Moriyama et al., Nitric oxide-mediated vasodilatation is decreased in forearm resistance vessels in patients with coronary spastic angina, JPN CIRC J, 65(2), 2001, pp. 81-86
Citations number
48
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION
ISSN journal
0047-1828 → ACNP
Volume
65
Issue
2
Year of publication
2001
Pages
81 - 86
Database
ISI
SICI code
0047-1828(200102)65:2<81:NOVIDI>2.0.ZU;2-I
Abstract
It has been reported that coronary endothelial dysfunction is associated wi th the pathogenesis of coronary spasm, and that endothelial nitric oxide (N O) mediated vasodilatation was decreased in coronary epicardial arteries in patients with coronary spastic angina (CSA). However, there are few report s about the endothelial function in peripheral resistance vessels of patien ts with CSA, so the present study investigated the role of NO in forearm re sistance vessels in such patients. The responses of forearm blood flow to a cetylcholine (ACh; 8-24 mug/min) and sodium nitroprusside (SNP; 0.4-1.2 mug /ml) infusions was examined using plethysmography, and subsequently the res ponses to ACh after an infusion of N-G-monomethyl-L-arginine (L-NMMA; 4 mu mol/min, for 5 min) in 17 patients with CSA and 17 age- and sex- matched co ntrols. The vasodilator responses to ACh and SNP were comparable between th e 2 groups (p=NS). L-NMMA significantly suppressed the vasodilator response s to ACh in controls (p<0.05), but there was no significant difference in t he responses to ACh before and after infusion of L-NMMA in patients with CS A (p=NS). These results indicate that endothelial NO-mediated vasodilatatio n is decreased in the forearm resistance vessels of patients with CSA.