Mechanism of 5-HT contraction in isolated bovine ventricular coronary arteries. Evidence for transient receptor-operated calcium influx channels.

The effect of serotonin on isometric tension and transmembrane calcium influx was investigated in rings cut from branches of male bovine circumflex and left anterior descending coronary arteries. Responses were compared to those produced by potassium chloride, and to the serotonin contraction produced in rabbit thoracic aorta. Serotonin in bovine ventricular coronary arteries produced a strong, transient contraction, even at a maximum concentration. Contraction did not decline because of serotonin degradation in the bathing medium. The ability of serotonin to contract bovine ventricular coronary arteries was largely preserved when rings were exposed to a calcium-free medium. When calcium was replaced in the medium, both tension (T) and calcium influx (C, 45Ca) were increased above control only transiently by serotonin (3 minutes post-serotonin: T = 49.0 +/- 13.3 mg/mg, C = 27.33 +/- 1.8 mumol/kg, compared with control T = -4.8 +/- 1.5, C = 19.7 +/- 1.4; 30 minutes post-serotonin: T = -17.3 +/- 2.1, C = 19.3 +/- 1.1, compared with control T = -19.6 +/- 4.1, C = 18.1 +/- 1.4). Potassium chloride-stimulated increases in tension and calcium influx in bovine ventricular coronary arteries and a maximum serotonin contraction in rabbit thoracic aorta were not transient, but were sustained 30 minutes via a mechanism that appeared to be dependent on the influx of extracellular calcium. We suggest that the transient nature of the serotonin contraction in bovine ventricular coronary arteries was the result of a time-dependent decline in both calcium release from intracellular stores and calcium influx through serotonin receptor-operated calcium channels.(ABSTRACT TRUNCATED AT 250 WORDS)