Adenosine-stimulated ca2+ reabsorption is mediated by apical a1
receptors in rabbit cortical collecting system.
Hoenderop, Joost G. J., Anita Hartog, Peter H. G. M. Willems, and
Ren[acute]e J. M. Bindels.
Departments of Biochemistry and Cell Physiology, Institute of
Cellular Signalling, University of Nijmegen, The Netherlands
APStracts 5:0017F, 1998.
Confluent monolayers of immunodissected rabbit connecting tubule and
cortical collecting duct cells, cultured on permeable supports, were
used to study the effect of adenosine on net apical-to-basolateral
Ca2+ transport. Apical, but not basolateral, adenosine increased this
transport dose-dependently from 48 +/- 3 to 110 +/- 4 nmol.h-1.cm-2.
Although a concomitant increase in cAMP formation suggested the
involvement of an A2 receptor, the A2 agonist CGS 21680 did not
stimulate Ca2+ transport, while readily increasing cAMP. By contrast,
the A1 agonist CPA maximally stimulated Ca2+ transport without
significantly affecting cAMP. Adenosine-stimulated transport was
effectively inhibited by the A1 antagonist DPCPX, but not the A2
antagonist DMPX, providing additional evidence for the involvement of
an A1 receptor. Both abolishment of the adenosine-induced transient
increase in [Ca2+]i by BAPTA and down-regulation of PKC by prolonged
phorbol ester treatment were without effect on adenosine-stimulated
Ca2+ transport. The data presented suggest that adenosine interacts
with an apical A1 receptor to stimulate Ca2+ transport via a hitherto
unknown pathway that does not involve cAMP formation, PKC activation
and/or Ca2+ mobilization.
Received 23 July 1997; accepted in final form 8 January 1998.
APS Manuscript Number F241-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 28 January 1998