Egf modulation of na/h antiport in rat hepatocytes: different
sensitivity in adult and fetal cells.
Incerpi, S., S. Spagnuolo, F. Terenzi, and S. Leoni.
Department of Cellular and Developmental Biology, University of
Rome 'La Sapienza', piazzale Aldo Moro, 00185 Rome, Italy and
Department of Biology, University of Rome 'Tor Vergata', via della
Ricerca Scientifica, 00133 Rome, Italy
APStracts 2:0330C, 1995.
The modulation by EGF of the Na/H antiport in fetal and adult rat
hepatocytes was studied in nominally HCO3--free solution. EGF (10 nM)
activated the antiport in adult rat hepatocytes by 0.22+0.03
(mean+SD; n=10) pH units over basal value, measured with the
fluorescent, pH-sensitive intracellular probe, 2',7' bis
(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). The effect of EGF was
inhibited by amiloride analog 5-(N-ethyl-N-isopropyl) amiloride
(EIPA), by ouabain, inhibitor of the sodium pump, and by erbstatin
analog, an inhibitor of the tyrosine kinase activity of the EGF
receptor. The effect of EGF on Na/H antiport in adult rat hepatocytes
appeared to be mediated by both protein kinase C (PKC) and G protein
system. No effect of EGF and PMA, an activator of PKC, on the Na/H
antiport was observed in fetal hepatocytes of 20 and 22 days. A
different sensitivity of the antiport to high concentrations of
amiloride and EIPA suggest that altered amount of tha Na/H antiport
units or different isoforms could be expressed in fetal compared to
adult cells.
Received 10 April 1995; accepted in final form 5 September 1995.
APS Manuscript Number C201-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.