Effects of calcium channel blockers on the contractility of the filariid Acanthocheilonema viteae.

The role of calcium in muscle contractility was explored in the filarial nematode Acanthocheilonema viteae (Dipetalonema viteae). The parasite was slit open longitudinally and mounted in a smooth-muscle chamber that had been filled with aerated (95% N2/5% CO2) physiological solution at 37 degrees C. Nifedipine (10(-6) M) and cadmium (3 x 10(-5) M) reduced the spontaneous isotonic contractions of A. viteae, whereas verapamil (10(-5) M) and diltiazem (10(-5) M) enhanced them. The effects of nifedipine and verapamil did not appear to be due to the solvent ethanol. All of the drugs reduced the maximal contraction induced by acetylcholine (ACh, 10(-5) M), although nifedipine was the most potent. After the exposure of worm preparations to a calcium-free medium containing ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA, 10(-4) M) for 1 h, application of ACh (10(-5) M) induced a small, transient contraction. Subsequent applications of ACh in this medium had no effect. Thus, the nematode muscle contraction appears to depend on extracellular calcium. Nifedipine, diltiazem, and verapamil could act by reducing the calcium influx across the muscle membrane.