ELECTRIC-FIELD STIMULATION-INDUCED GUINEA-PIG GALLBLADDER CONTRACTIONS - ROLE OF CALCIUM CHANNELS IN ACETYLCHOLINE-RELEASE

Gallbladder motility is modulated by intrinsic cholinergic neurons, Th e aims of this study were to determine: (1) the effect of electric fie ld stimulation (EFS) on guinea pig gallbladder smooth muscle, and (2) the role of calcium channels in mediating neurotransmitter release. Ga llbladder muscle strips were studied isometrically in vitro. EFS (1-16 Hz, 100 V, 0.5-msec pulse width, 30-sec train duration) was used to a ctivate the intrinsic nerves, Exogenous acetylcholine was also used to directly stimulate the smooth muscle, EFS produced a frequency-depend ent contractile response that was completely abolished by tetrodotoxin , EFS-induced contractions at 16 Hz were suppressed by 84 +/- 4% with atropine, whereas hexamethonium had no effect, The L-type calcium chan nel blocker, nifedipine, reduced EFS contractions by 51 +/- 4%, wherea s it reduced contractions to acetylcholine by only 11 +/- 5%, The N-ty pe calcium channel blocker, omega-conotoxin GVIA, reduced EFS-induced contractions by 22 +/- 9%, but did not affect acetylcholine-induced co ntractions. EFS-induced contractions of the guinea pig gallbladder are primarily mediated by activation of postganglionic cholinergic neuron s. The acetylcholine release from these cholinergic neurons is regulat ed by L- and N-type calcium channels, The inhibitory effect of calcium channel blockers on the gallbladder seen in vivo may be in part relat ed to inhibition of acetylcholine release from the intrinsic cholinerg ic nerves of the gallbladder.