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Acetylcholine‐induced coronary vasoconstriction was improved with supplementation of folic acid in hyperhomocysteinemic mice: an implication to coronary vasospasm
Author(s) -
Qipshidze Natia,
Tyagi Neetu,
Munjal Charu,
Metreveli Naira,
Lominadze David,
Tyagi Suresh C
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.819.1
Human atherosclerotic coronary vessels elicited vasoconstriction to acetylcholine (Ach). Since we showed that the levels of homocysteine are elevated in the atherosclerotic plaque tissue, we hypothesized that hyperhomocysteinemia damages endothelium and proliferates smooth muscle cells, causing narrowing of the vascular lumen and leading to vasospasm. Hyperhomocysteinemic‐cystathionine beta synthase‐heterozygote (CBS−/+) and wild type (CBS+/+) mice were treated with or without folic acid (FA) in drinking water for 4 weeks. Isolated mouse septum coronary artery was cannulated and pressurized at 60 mmHg. The vessels were treated with Ach (10 −10 ‐ 10 −5 M) and, for comparison, with nonendothelial vasodilator sodium nitroprusside (10 −5 M). Endothelium‐damaged vessels constricted in response to Ach and this vasoconstriction was improved with FA supplementation. Level of eNOS was lower in coronary artery in CBS−/+ than in control. Treatment with FA improved the level of eNOS in coronary artery of CBS−/+ mice. These results suggest that in isolated mouse coronary artery endothelial dysfunction causes vasoconstriction induced by Ach and the treatment with FA improves the Ach‐induced vasoconstriction in CBS−/+ mice. In conclusion FA supplementation restores endothelial function through amelioration of eNOS dysfunction, and may mitigate Ach‐induced coronary vasoconstriction.