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Characterization of muscarinic receptor subtype mediating contraction and relaxation in equine coronary artery in vitro
Author(s) -
OBI T.,
KABEYAMA A.,
NISHIO A.
Publication year - 1994
Publication title -
journal of veterinary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.527
H-Index - 60
eISSN - 1365-2885
pISSN - 0140-7783
DOI - 10.1111/j.1365-2885.1994.tb00237.x
Subject(s) - pirenzepine , methoctramine , muscarinic acetylcholine receptor , contraction (grammar) , acetylcholine , phenylephrine , chemistry , muscarinic acetylcholine receptor m3 , endocrinology , medicine , endothelium , receptor , biology , blood pressure
In coronary arterial rings isolated from horses, 10‐ ‐8 ‐10 ‐6 mol/l acetylcholine (ACh) induced concentration‐dependent contractions which were potentiated by the removal of endothelium and by pretreatment with I,‐nitro‐arginine (LNAG) or methylene blue (MB). Relatively lower concentrations of Ach 10‐ 14 ‐10‐ 8 mol/l) induced relaxation when the coronary rings were contracted by phenylephrine (PE). ACh‐induced contractions in the coronary rings without endothelium were competitively inhibited by each muscarinic subtype selective antagonist in the following order of potency: 4‐diphenylacetoxy‐N‐methylpiperidine methiodide (4‐DAMP) > pirenzepine ≥ parafluoro‐hexahydrosiladiphenidol (pFHHSiD) > methoctramine. ACh‐induced relaxation in the rings with endothelium was inhibited by LNAG or MB, and by each selective antagonist in the following order of potency: 4‐DAMP < pFHHSiD ≥ pirenzepine ≥ methoctramine. These results suggest that the ACh‐induced contraction and relaxation in equine coronary arteries are mediated mainly by an M 3 ‐receptor located on the smooth muscle cells and endothelial cells, respectively, and that the stimulation of the M 3 ‐receptor on the endothelial cells liberates nitric oxide.