Effect of epinephrine on camp accumulation in cultured rat inner
medullary collecting duct cells.
Yasuda, Gen, Satoshi Umemura, and William B. Jeffries.
Second Department of Internal Medicine, Yokohama City University
School of Medicine, Yokohama, 232 Japan, Department of Pharmacology,
Creighton University School of Medicine, Omaha, Nebraska, 68131
APStracts 3:0207F, 1996.
In a previous study we have reported the existence of [alpha]2- and
[beta]- adrenoceptors in cultured rat inner medullary collecting duct
(IMCD) cells. In this report, we examined the effect of epinephrine
on intracellular adenosine 3', 5'-cyclic monophosphate (cAMP)
accumulation and evaluated whether [alpha]2-adrenoceptors interact
with [beta]-, vasopressin-, and prostaglandin (PG) E2-receptors by
measuring cAMP generation. Epinephrine stimulated cAMP accumulation
in a dose-dependent manner (EC50 = 300 nM). Rauwolscine (10 [mu]M)
enhanced epinephrine-effects, shifting the dose-response curve for
epinephrine to the left (EC50 = 120 nM), however, [beta]-antagonists
inhibited epinephrine-induced cAMP accumulation. Epinephrine (10
[mu]M) inhibited cAMP accumulation maximally induced by isoproterenol
(10 [mu]M); this effect was reversed by rauwolscine (10 [mu]M).
Epinephrine inhibited vasopressin (100 nM)-induced cAMP accumulation
but failed to inhibit PGE2 (10 [mu]M)-induced cAMP accumulation. We
conclude that epinephrine acts as an [alpha]2- and [beta]
-adrenoceptor agonist, and that [alpha]2-adrenoceptors interact with
[beta]- and vasopressin-receptors but not with PGE2-receptors on cAMP
accumulation. This suggests that [alpha]2-adrenoceptors play a
physiological role via interaction with different hormone receptors.
Received 8 May 1996; accepted in final form 7 November 1996.
APS Manuscript Number F141-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996