Key result
Acetylcholine blocks forskolin and theophylline-induced electrophysiological effects and cAMP elevation via adenylate cyclase inhibition.
Acetylcholine modulates the effects of secretagogues in Necturus gallbladder epithelium by inhibiting adenylate cyclase via a PTX-sensitive G protein.
Acetylcholine may inhibit adenylate cyclase in gallbladder epithelium; leaves open relevance to human biliary secretion.
Elevation of adenosine 3',5'-cyclic monophosphate (cAMP) levels in Necturus gallbladder (NGB) epithelium activates an apical membrane Cl- conductance and decreases transepithelial fluid transport (Jv). Acetylcholine (ACh), which had no effects on Jv by itself, antagonized the electrophysiological effects of forskolin (FSK) and theophylline and the decrease in Jv produced by FSK. By itself, ACh had no effects on basal cAMP levels but antagonized the increases in cAMP induced by FSK and theophylline. ACh had no effect on phosphodiesterase activity and prevented both the electrophysiological response and the elevation in cAMP by theophylline. In conclusion, the effect of ACh is mediated by inhibition of adenylate cyclase. A pertussis toxin (PTX)-sensitive G protein may mediate inhibition of adenylate cyclase because pretreatment with PTX prevented the reversal of the electrophysiological effects of FSK by ACh, and PTX catalyzed the ribosylation of cell membranes from NGB epithelium. ACh could have a physiological role in modulating the effects of secretagogues that act via elevation of cAMP levels.
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Altenberg et al. (1994) studied this question. Acetylcholine vs. Forskolin and theophylline alone was evaluated on cAMP levels and electrophysiological effects. Acetylcholine antagonized the electrophysiological effects and cAMP elevation induced by forskolin and theophylline in Necturus gallbladder epithelium via inhibition of adenylate cyclase.
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