[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.