PGE(2) activation of apical membrane Cl- channels in A6 epithelia: Impedance analysis

Measurements of transepithelial electrical impedance of continuously short- circuited A6 epithelia were made at audio frequencies (0.244 Hz to 10.45 kH z) to investigate the time course and extent to which prostaglandin E-2 (PG E(2)) modulates Cl- transport and apical membrane capacitance in this cell- cultured model epithelium. Apical and basolateral membrane resistances were determined by nonlinear curve-fitting of the impedance vectors at relative ly low frequencies (< 50 Hz) to equations (Paunescu, T. G., and S. I. Helma n. 2001. Biophys. J. 81:838-851) where depressed Nyquist impedance semicirc les were characteristic of the membrane impedances under control Na+-transp orting and amiloride-inhibited conditions. In all tissues (control, amilori de-blocked, and amiloride-blocked and furosemide-pretreated), PGE(2) caused relatively small (< similar to3 muA/cm(2)) and rapid (< 60 s) maximal incr ease of chloride current due to activation of a rather large increase of ap ical membrane conductance that preceded significant activation of Na+ trans port through amiloride-sensitive epithelial Na+ channels (ENaCs). Apical me mbrane capacitance was frequency-dependent with a Cole-Cole dielectric disp ersion whose relaxation frequency was near 150 Hz. Analysis of the time-dep endent changes of the complex frequency-dependent equivalent capacitance of the cells at frequencies >1.5 kHz revealed that the mean 9.8% increase of capacitance caused by PGE(2) was not correlated in time with activation of chloride conductance, but rather correlated with activation of apical membr ane Na+ transport.