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2-induced inhibition
of AVP- and cAMP-stimulated H2O, Na+,
and urea transport in rat IMCD
1 Oklahoma State University College of Osteopathic Medicine, Tulsa, Oklahoma 74107; and 2 Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil 01246
PGE2 inhibits osmotic water
permeability (Pf) in the rat inner medullary
collecting duct (IMCD) via cellular events occurring after the
stimulation of cAMP, i.e., post-cAMP-dependent events. The
2-agonists also inhibit Pf in the
rat IMCD via post-cAMP-dependent events. The purpose of this study was
to determine whether PGE2 plays a role in
2-mediated inhibition of Pf,
Na+, and urea transport in the rat IMCD. Isolated terminal
IMCDs from Wistar rats were perfused to measure, in separate
experiments, Pf, lumen-to-bath
22Na+ transport (Jlb),
and urea permeability (Pu). Transport was
stimulated with 220 pM arginine vasopressin (AVP) or 0.1 mM
8-(4-chlorophenylthio)-cAMP (CPT-cAMP). Indomethacin was used to
inhibit endogenous prostaglandin synthesis, and the
2-agonists clonidine, oxymetazoline, and dexmedetomidine were used to test the role of PGE2 in the
2-mediated mechanism that inhibits transport. All agents
were added to the bath. Indomethacin at 5 µM significantly elevated
CPT-cAMP-stimulated Pf,
Jlb, and Pu, and
subsequent addition of 100 nM PGE2 reduced these transport parameters. Indomethacin reversed 2 inhibition of
CPT-cAMP-stimulated Pf,
Jlb, and Pu, and
subsequent addition of PGE2 reduced transport in each case.
Indomethacin partially reversed 2 inhibition of AVP-stimulated Pf, Jlb,
and Pu, and PGE2 reduced transport
back to the 2-inhibited level. These results indicate
that PGE2 is a second messenger involved in the mechanism
of transport inhibition mediated by 2-adrenoceptors via
post-cAMP-dependent events in the rat IMCD.
signaling pathways; second messengers; inner medullary collecting
duct; 2-adrenoceptor; osmotic water permeability
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