Lc. Martin et al., ELECTROGENIC BICARBONATE SECRETION IN MOUSE GALLBLADDER, American journal of physiology: Gastrointestinal and liver physiology, 37(6), 1998, pp. 1045-1052
Mouse gallbladders (4 mm(2)) were investigated using the short-circuit
current (I-sc) technique. Responses of 50 mu A/cm(2) were obtained in
response to forskolin and agents that stimulated the adenylate cyclas
e system (IBMX and dibutyryl-cAMP). The calcium ionophore ionomycin in
creased I-sc to 30% of the forskolin-stimulated increase. The forskoli
n-dependent current was inhibited 40% by acetazolamide but was insensi
tive to furosemide. Forskolin responses were dependent on the presence
of bicarbonate ions; removal from both sides of the membrane or the b
asolateral side alone caused a significant reduction in responses. Rem
oval of chloride ions from the basolateral side had no effect, while r
emoval from the apical side caused a significant reduction in the fors
kolin responses, but only by 30%. It is argued that the remaining curr
ent (70%) cannot result from a parallel arrangement of a chloride chan
nel and a chloride-bicarbonate exchanger and that bicarbonate is secre
ted through the apical membrane by a predominantly conductive mechanis
m. Apparently, forskolin converts a near electrically silent epitheliu
m to an electrogenically secreting tissue.