Contractility of isolated human epicardial coronary artery segments. A clue to the mechanism of coronary spasm underlying angina pectoris.

Isolated segments of human epicardial coronary arteries excised 3-5 hours after sudden cardiac death demonstrated spontaneous contractility. This contractility was abolished by Ca-free solution, Ca-antagonists, sodium nitroprusside or beta-adrenoceptor stimulation. Maximum increase in tension produced by norepinephrine (with beta-adrenoceptor blocker) was half of the maximum tension induced by acetylcholine or histamine. Coronary segments with severe atherosclerotic lesions failed to relax in response to high concentrations of norepinephrine while the activation of spontaneous rhythmicity produced by low concentrations of the amine and acetylcholine, histamine or serotonin was retained. Under high initial tone, at room temperature of the bath solution or potassium depolarization when phasic contractions were abolished, human coronary segments responded to agonists with a dose-dependent increase in tension. Activation of contraction through P- and T-systems and to role of extracellular and intracellular Ca-stores in the mechanism of human coronary smooth muscle regulation are discussed.