To study the direct effect of somatostatin (SS) on calcium channel current (IBa) in guinea-pig gastric myocytes, IBa was recorded by using whole-cell patch clamp technique in single smooth muscle cells. Nicardipine (1μM), a L-type Ca2+ channel blocker, inhibited IBa by 98⁑1.9% (n=5), however IBa was decreased in a reversible manner by application of SS. The peak IBa at 0 mV were decreased to 95⁑1.1, 92⁑1.9, 82⁑4.0, 66⁑5.8, 10⁑2.9% at 10⁣10, 10⁣9, 10⁣8, 10⁣7, 10⁣5 M of SS, respectively (n=3∼6; mean⁑SEM). The steady-state activation and inactivation curves of IBa as a function of membrane potentials were well fitted by a Boltzmann equation. Voltage of half-activation (V0.5) was ⁣12⁑0.5 mV in control and ⁣11⁑1.9 mV in SS treated groups (respectively, n=5). The same values of half-inactivation were ⁣35⁑1.4 mV and ⁣35⁑1.9 mV (respectively, n=5). There was no significant difference in activation and inactivation kinetics of IBa by SS. Inhibitory effect of SS on IBa was significantly reduced by either dialysis of intracellular solution with GDPβS, a non-hydrolysable G protein inhibitor, or pretreatment with pertussis toxin (PTX). SS also decreased contraction of guinea-pig gastric antral smooth muscle. In conclusion, SS decreases voltage-dependent L-type calcium channel current (VDCCL) via PTX- sensitive signaling pathways in guinea-pig antral circular myocytes.