DOPAMINE ACTIVATES APICAL MEMBRANE CL- CONDUCTANCE AND INHIBITS FLUIDABSORPTION IN AMPHIBIAN GALLBLADDER BY ELEVATING INTRACELLULAR CAMP

Addition of dopamine to the solution bathing the basolateral surface o f Necturus gallbladder (NGB) caused cell membrane depolarization, a fa ll in the apparent electrical resistance of the apical membrane, a tra nsient depolarizing response to a reduction in apical solution [Cl-], and a decrease in transepithelial fluid absorption. These results are consistent with a dopamine-mediated increase in apical membrane Cl- co nductance (G(Cla)). The half-maximal concentration for the effect of d opamine was approximately 1 mu M. Most experiments were carried out wi th 10 mu M. The effects of dopamine were abolished by a D-1 receptor a ntagonist, and unchanged by a D-2 receptor antagonist. Dopamine produc ed a similar to 10-fold increase in cAMP tissue content. Because in NG B epithelium acetylcholine (ACh) inhibits adenylate cyclase via an inh ibitory G protein [Altenberg et al.: Am. J. Physiol., in press], we te sted the effect of ACh on the response to dopamine. ACh (10 mu M, baso lateral solution) abolished the effects of dopamine on fluid absorptio n, G(Cla) and cAMP levels. We conclude that in NGB epithelium dopamine activates G(Cla) by stimulation of D-1-like receptors. This causes st imulation of adenylate cyclase and elevation of intracellular cAMP. Th e effects of dopamine are abolished by acetylcholine, which inhibits a denylate cyclase.