{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,2]],"date-time":"2025-07-02T18:47:07Z","timestamp":1751482027282},"reference-count":37,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2011,7,22]],"date-time":"2011-07-22T00:00:00Z","timestamp":1311292800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2011,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Human atherosclerotic coronary vessels elicited vasoconstriction to acetylcholine (Ach) and revealed a phenomenon of vasospasm. Homocysteine (Hcy) levels are elevated in the atherosclerotic plaque tissue, suggesting its pathological role in endothelial damage in atherosclerotic diseases. Accordingly, we examined the role hyperhomocysteinemia in coronary endothelial dysfunction, vessel wall thickness, lumen narrowing, leading to acute\/chronic coronary vasospasm. The therapeutic potential and mechanisms of folic acid (FA) using hyperhomocysteinemic cystathionine beta synthase heterozygote (CBS\u2212\/+) and wild type (CBS+\/+) mice were addressed. The CBS\u2212\/+ and CBS+\/+ mice were treated with or without a Hcy lowering agent FA in drinking water (0.03\u2009g\/L) for 4 weeks. The isolated mouse septum coronary artery was cannulated and pressurized at 60\u2009mmHg. The wall thickness and lumen diameters were measured by Ion\u2010Optic. The vessels were treated with Ach (10<jats:sup>\u22128<\/jats:sup>\u201310<jats:sup>\u22125<\/jats:sup>\u2009M) and, for comparison, with non\u2010endothelial vasodilator sodium nitroprusside (10<jats:sup>\u22125<\/jats:sup>\u2009M). The endothelium\u2010impaired arteries from CBC\u2212\/+ mice constricted in response to Ach and this vasoconstriction was mitigated with FA supplementation. The level of endothelial nitric oxide synthase (eNOS) was lower in coronary artery in CBS\u2212\/+ than of CBS+\/+ mice. Treatment with FA increased the levels of Ach\u2010induced NO generation in the coronary artery of CBS\u2212\/+ mice. The results suggest that Ach induced coronary vasoconstriction in CBS\u2212\/+ mice and this vasoconstriction was ameliorated by FA treatment. The mechanisms for the impairment of vascular function and therapeutic effects of FA may be related to the regulation of eNOS expression, NO availability and tissue homocysteine. J. Cell. Physiol. 226: 2712\u20132720, 2011. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.22621","type":"journal-article","created":{"date-parts":[[2010,12,30]],"date-time":"2010-12-30T13:07:52Z","timestamp":1293714472000},"page":"2712-2720","source":"Crossref","is-referenced-by-count":15,"title":["Folic acid improves acetylcholine\u2010induced vasoconstriction of coronary vessels isolated from hyperhomocysteinemic mice: An implication to coronary vasospasm"],"prefix":"10.1002","volume":"226","author":[{"given":"Natia","family":"Qipshidze","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naira","family":"Metreveli","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Lominadze","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Suresh 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