Transport Processes, Metabolism and Endocrinology; Kidney, Gastrointestinal Tract, and Exocrine Glands
Cite this article as:
Flonta, ML., Galter, D., Frangopol, P.T. et al. Pflugers Arch. (1987) 408: 215. doi:10.1007/BF02181461
Procaine has opposite effects on the active transport of Na+ when applied on the mucosal side of the frog skin [where it produces a stimulation of the short-circuit current (Isc)] or when added on the serosal side (where it produces an inhibition ofIsc). In an attempt to reveal and localize the primary effect of procaine on either the apical or latero-basal membranes of the epithelial cells, we have tried to “chemically dissect” both membrane functions with inhibitors and ionophores. When applied on the apical side of the latero-basally depolarized epithelium, 25 mmol/l procaine increasesIsc andVoc (transepithelial open-circuit potential), while decreasing the transepithelial resistance. TheE1−E2 linearity domain of the I–V curves is narrowed. On the serosal side of the depolarized epithelium, the same concentration of procaine does not affectIsc andVoc (which are already inhibited) but it produces an increase in the transepithelial resistance (Rt). Procaine influence on the passive K+ permeability was studied by using the ionophore nystatin, which is assumed to form channels permeable to K+, when applied on the amiloride blocked apical membrane. In nystatin-treated epithelia, 25 mmol/l procaine on the apical side decreaseIsc,Voc andRt. In parallel experiments during Cl− substitution by SO42−, the procaine effects onIsc andVoc are no longer maintained, but transient. The results suggest that procaine positively influences the Na+ transient through the apical Na+-channels, and inhibits the epithelial permeability for K+, possibly by reducing K+-ions accessibility to the K+-channels.