Regulation of L-type Calcium Channel Current by Somatostatin in Guinea-Pig Gastric Myocytes

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 (1microM), 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 GDPbetaS, 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.

Inwardly Rectifying K+ Currents in Gastric Myocytes of Guinea-pig

To identify the presence of inwardly rectifying K+ channels and its characteristics, membrane currents were measured using a whole-cell patch clamp from isolated gastric myocytes of guinea-pig. Change of external K+ concentration from 5 to 90 mM induced an inward current at a holding potential of 80 mV. The high K+-induced inward current was blocked by Ba2+ and Cs+, but not by glibenclamide. With 90 mM K+ in bath, the Ba2+- and Cs+-sensitive currents showed strong inward rectification. Ten mM TEA weakly blocked the inward current only at potentials more negative than 50 mV. With 90 mM K+ in bath, hyperpolarizing step pulses from 10 mV induced inward currents, which were inactivated at potentials more negative than 70 mV. Reduction of external K+ to 60 mM decreased the amplitudes of the currents and shifted the reversal potential to more negative potential. The inactivation of inward K+ current at negative clamp voltage was not affected by removing external Na . These results suggest that the inwardly rectifying K+ channels may exist in gastric smooth muscle.