Atp-induced rise in apamin-sensitive ca2+-dependent k+ conductance
in adult rat hepatocytes.
Yamashita, Yoshiro, Hisashi Ogawa, and Norio Akaike.
Department of Physiology, Kyushu University Faculty of Medicine,
Fukuoka 812-82, the Department of Physiology, Kumamoto University
School of Medicine, Kumamoto 860, Japan
APStracts 2:0178G, 1995.
Exogenous ATP-induced transient outward currents ( IATPs) were
investigated in isolated adult rat hepatocytes using conventional
whole-cell patch and nystatin-perforated patch recording modes. The
IATP increased in a sigmoidal fashion with an increase in ATP
concentration, where the half-maximal concentration was 1.4 [mu]M.
The order of current potency was 2-methylthio-ATP >/= UTP = ATP
>> a,b-methylene-ATP. IATP was depressed in a
concentration-dependent manner by suramin and apamin. IATP reversed
its direction at the K+ equilibrium potential. IATP occurred easily
in hepatocytes obtained from female rats weighing more than 250 g.
Removal of extracellular Ca2+ had no effect on the peak amplitude of
IATP, but thapsigargin abolished it. Intracellular perfusion with
BAPTA, heparin, GTP[gamma]S or neomycin also abolished IATP.
Pretreatment with pertussis toxin or calmodulin antagonists had no
effect on IATP. It was concluded that ATP-binding to both P2Y and P2U
purinoceptors coupled to G-protein may raise apamin-sensitive Ca2+
-dependent K+ conductance via a phospholipase C-inositol
trisphosphate-Ca2+ signaling pathway.
Received 3 October 1994; accepted in final form 25 August 1995.
APS Manuscript Number G389-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.