Effects of diltiazem on electrical responses evoked spontaneously or by electrical stimulation in the antrum smooth muscle cells of the guinea-pig stomach.

In circular smooth muscle cells of the guinea-pig stomach (antrum), diltiazem (10(-6)-10(-5)M) blocked the overshooting spike potential generated either spontaneously or by electrical stimulation in the presence of 2 mM tetraethylammonium chloride, but did not block the slow wave and the abortive spike potential. The membrane was depolarized by high concentrations of diltiazem (more than 3 X 10(-6)M), and this depolarization was associated with an increase in the membrane resistance. The interval between slow waves was shortened to about 0.90 times the control (14.7s) by 10(-5)M diltiazem. Transmural nerve stimulation evoked an inhibitory junction potential (i.j.p.) and enhanced the subsequently generated slow wave. Tetrodotoxin (3 X 10(-7)M) blocked both responses but atropine (10(-6)M) blocked only the latter. Diltiazem (more than 10(-6)M) increased the amplitude of the i.j.p. and depressed the enhancement of the slow wave produced by transmural nerve stimulation, presumably due to depolarization of the membrane. The latency for the i.j.p. remained the same in the presence of diltiazem (10(-5)M). It is concluded that in the guinea-pig stomach, diltiazem blocks Ca-influx during the generation of the overshooting spike potential, but not the Ca-influx related to generation of the abortive spike potential or the slow wave. The cholinergic excitatory and the non-adrenergic, non-cholinergic inhibitory transmission may not be much affected by diltiazem.