Contractile activity of human coronary arteries and human myocardium in vitro and their sensitivity to calcium entry blockade by nifedipine.

Depolarization (100 mM K+) of acetylcholine, serotonin and prostaglandin (PG) F2 alpha contracted human isolated coronary artery segments. Serotonin was about 10-fold more potent than either acetylcholine or PGF2 alpha, but PGF2 alpha elicited contractions of the greatest magnitude. Serotonin (10 microM) and PGF2 alpha (3 microM) induced rhythmic contractions in the arterial segments. Depolarization-, PGF2 alpha- and serotonin-induced increase in tone was depressed by nifedipine, as was the serotonin- and PGF2 alpha -induced rhythmic activity. The induced rhythmic activity was about 100-fold more sensitive to inhibition by nifedipine than was the induced tonic contraction of the arteries. Depolarization-induced contractions and serotonin-induced rhythmic contractions displayed about equal sensitivity to inhibition by nifedipine. Nifedipine was more potent as an inhibitor of depolarization-induced contractions of arteries than it was as an inhibitor of electrically stimulated trabecular strips of ventricle from the same hearts. The inhibition of isolated coronary artery contraction was obtained within the range of nifedipine concentrations observed in the blood of treated patients.