Activation of an amiloride sensitive conductance by the apical
adenosine receptor in a human intestinal cell line.
Bouritius, Hetty, and Jack A. Groot.
GRADUATE SCHOOL NEUROSCIENCES AMSTERDAM, INSTITUTE OF NEUROBIOLOGY,
BIOLOGICAL FACULTY, UNIVERSITY OF AMSTERDAM, KRUISLAAN 320, 1098 SM
AMSTERDAM, THE NETHERLANDS
APStracts 3:0335C, 1996.
We studied the effects of stimulation of the apical adenosine receptor
on ion transport by HT29cl.19A cells, with the conventional
microelectrode technique. Adenosine (100 [mu]M) caused an increase in
the transepithelial potential (aeyt=3.6+/-0.4 mV) and equivalent
short circuit current (aeeq.Isc=21+/-3 [mu]A/cm2), a transient
depolarization of the membrane potential (aeya=14+/-2 mV) and
decrease of the apical membrane resistance. The increase in eq.Isc
was additive to the effect of forskolin or basolateral addition of a
maximal concentration of adenosine. Bumetanide, applied after
adenosine, caused a further depolarization (7+/-2 mV), concomitant
with a decrease of eq.Isc (-13+/-2 [mu]A/cm2) and an increase of the
basolateral membrane resistance. Substitution of Cl- with gluconate
or Na+ with N-methylglucamine reduced the response to adenosine with
more than 60%. The response was also reduced by a low concentration
of amiloride. We conclude that stimulation of the apical adenosine
receptor activated a cation conductance in the apical membrane.
Received 5 Decenber 1995; accepted in final form 8 October 1996.
APS Manuscript Number C728-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996