Effects of calcium channel blockers on pharmacologically induced contractions of rainbow trout (Oncorhynchus mykiss) intestine.

Calcium depletion/replacement studies were carried out to examine the role of calcium in contraction of trout intestinal smoot muscle in vitro. Three chemically distinct calcium channel blockers were used to determine whether voltage operated calcium channels (VOCs) were involved in calcium entry with either agonist or depolarization-induced contractions. Contractions induced by depolarizing intestinal smooth muscle with potassium were totally dependent on extracellular calcium, whereas receptor-mediated responses to 5-hydroxytryptamine (5-HT) and carbachol also relied on calcium derived from intracellular stores. The calcium channel blockers, verapamil, nitrendipine, and diltiazem, all shifted the calcium-response curve for potassium to the right, supporting the existence of VOCs in trout intestinal smooth muscle. The calcium-response curve for 5-HT was also shifted to the right, suggesting that 5-HT can induce calcium uptake into the smooth muscle via VOCs, in addition to mobilizing intracellular calcium. Verapamil also appeared to block 5-HT receptors directly. Carbachol-induced contractions were only reduced by diltiazem at low concentrations of calcium (0.1-1 mM), suggesting that diltiazem has some other mechanisms of action than the other calcium channel blockers. Activation of muscarinic receptors may induce calcium entry through channels other than the VOCs, in addition to mobilizing intracellular calcium.