Electrophysiology and noise analysis of K+-depolarized epithelia of frog skin.

Epithelia of frog skin bathed either symmetrically with a sulfate-Ringer solution or bathed asymmetrically and depolarized with a 112 mM K+ basolateral solution (Kb+) were studied with intracellular microelectrode techniques. Kb+ depolarization caused an initial decrease of the short-circuit current (Isc) with a subsequent return of the Isc toward control values in 60-90 min. Whereas basolateral membrane resistance (Rb) and voltage were decreased markedly by high [Kb+], apical membrane electrical resistance (Ra) was decreased also. After 60 min, intracellular voltage averaged -27.3 mV, transcellular fractional resistance (fRa) was 86.8%, and Ra and Rb were decreased to 36.1 and 13.0%, of their control values, respectively. Amiloride-induced noise analysis of the apical membrane Na+ channels revealed that Na+ channel density was increased approximately 72% while single-channel Na+ current was decreased to 39.9% of control, roughly proportional to the decrease of apical membrane voltage (34.0% of control). In control and Kb+-depolarized epithelia, the Na+ channel density exhibited a phenomenon of autoregulation. Inhibition of Na+ entry (by amiloride) caused large increases of Na+ channel density toward saturating values of approximately 520 X 10(6) channels/cm2 in Kb+-depolarized tissues.

[1]  RS Fisher,et al.  Microelectrode studies of the active Na transport pathway of frog skin , 1977, The Journal of general physiology.

[2]  S. Lewis,et al.  Incorporation of cytoplasmic vesicles into apical membrane of mammalian urinary bladder epithelium , 1982, Nature.

[3]  B. Lindemann,et al.  Sodium-specific membrane channels of frog skin are pores: current fluctuations reveal high turnover. , 1977, Science.

[4]  T. Biber,et al.  Exposure of the isolated from skin to high potassium concentrations at the internal surface. I. Bioelectric phenomena and sodium transport. , 1963, The Journal of clinical investigation.

[5]  B. Minsky,et al.  Morphometric analysis of the translocation of lumenal membrane between cytoplasm and cell surface of transitional epithelial cells during the expansion-contraction cycles of mammalian urinary bladder , 1978, The Journal of cell biology.

[6]  P. Devreotes,et al.  Turnover of acetylcholine receptors in skeletal muscle. , 1976, Cold Spring Harbor symposia on quantitative biology.

[7]  B. Lindemann Fluctuation analysis of sodium channels in epithelia. , 1984, Annual review of physiology.

[8]  S. I. Helman,et al.  Autoregulation of apical membrane Na+ permeability of tight epithelia. Noise analysis with amiloride and CGS 4270 , 1985, The Journal of general physiology.

[9]  J. Wade,et al.  ADH ACTION: EVIDENCE FOR A MEMBRANE SHUTTLE MECHANISM * , 1981, Annals of the New York Academy of Sciences.

[10]  B. Lindemann,et al.  Current—voltage curve of sodium channels and concentration dependence of sodium permeability in frog skin , 1977, The Journal of physiology.

[11]  S. I. Helman,et al.  Hormonal control of apical membrane Na transport in epithelia. Studies with fluctuation analysis , 1983, The Journal of general physiology.

[12]  Q. Al-Awqati,et al.  Exocytosis regulates urinary acidification in turtle bladder by rapid insertion of H+ pumps into the luminal membrane. , 1982, Proceedings of the National Academy of Sciences of the United States of America.