Active sodium transport and fluid secretion in the gall‐bladder epithelium of Necturus.

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Abstract
Intracellular Na, K and Cl activities .**GRAPHIC**. .**GRAPHIC**. and .**GRAPHIC**. and membrane potentials were measured in Necturus gall-bladder epithelium using double-barrelled ion-sensitive micro-electrodes. Mucosal membrane potential was about -55 mV and the mean control activities were .**GRAPHIC**. = 14.7 mM, .**GRAPHIC**. = 91.6 mM and .**GRAPHIC**. = 20.3 mM. Replacing mucosal Na by K caused a fall in .**GRAPHIC**. that followed an exponential time course. The rate of change in .**GRAPHIC**. was linearly related to .**GRAPHIC**. above a certain value (.simeq. 3 mM). .**GRAPHIC**. and .**GRAPHIC**. both increased in K Ringer solution. From the change in all 3 ions, the cell was estimated to swell at an initial rate of 0.13% s-1. From the initial rate of change in .**GRAPHIC**. a net cell efflux of Na of 405 pmol cm-2 s-1 was calculated. Replacement of Na by Tris or choline led to a similar result. The transepithelial Na transport rate was for this group of animals 346 pmol cm-2 s-1. Ouabain (10-3 M) produced an increase in .**GRAPHIC**. and .**GRAPHIC**. whereas .**GRAPHIC**. decreased. The cells were estimated to swell at an initial rate of 0.06% s-1. The initial Na influx after Na-pump inhibition was calculated to be 162 pmol cm-2 s-1. The parallel measure of the transepithelial rate of transport of Na gave a value of 189 pmol cm-2 s-1. Ouabain inhibited the decrease in .**GRAPHIC**. after replacement of Na by K by about 80%. A fast depolarization, ranging from 2 to 7 mV, occurred after the perfusion with ouabain. Em then slowly decreased from about 53 to 32 mV in 1 h. Evidently, the major fraction of the transepithelial transport of Na is transcellular and mediated by the Na pump, the pumping rate is linearly dependent on internal Na within a certain range. The Na pump is electrogenic under normal circumstances.