[Cellular mechanisms of hypoxic coronary spasm].
Transient hypoxic contraction (THC) of vascular smooth muscle (VSM) of isolated human, canine and porcine coronary artery rings was preserved in Ca2+--free solution and abolished with procaine. The data obtained suggest that the THC of the coronary VSM is mediated via a Ca2+ release from sarcoplasmic reticulum under the effect of inositol-1,4, 5-triphosphate and may be triggered by action of endogenous noradrenaline on alpha 1-adrenoceptors. The mechanism of beta-adrenergic relaxation was not actualized in the hypoxia because of uncoupling of the beta-adrenoceptors from adenylate cyclase.
Solov'ev
A I
AI
D000818:Animals; D002118:Calcium / Q000378:metabolism; D003329:Coronary Vasospasm / Q000209:etiology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D004285:Dogs; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology; D009638:Norepinephrine / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000502:physiology / Q000648:ultrastructure; D013552:Swine
D007295:Inositol Phosphates; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium; D009638:Norepinephrine
Kletochnye mekhanizmy gipoksicheskogo koronarospazma.