Modulation of beta adrenergic receptor-stimulated lipolysis in the
heart by prostaglandins.
Ruan, Ying, Hong Kan, Climaco Cano, and Kafait U. Malik.
Department of Pharmacology, School of Medicine, University of
Tennessee, Memphis, TN 38163
APStracts 3:0106E, 1996.
The purpose of the present study was to investigate the contribution
of prostaglandins (PGs) to lipolysis elicited by beta adrenergic
receptor activation in the heart. We have studied the effect of PGE2,
PGI2, and their precursor, arachidonic acid (AA), in the presence and
absence of a cyclooxygenase inhibitor, sodium meclofenamate, on
glycerol output elicited by stimulation of beta adrenergic receptors
in the isolated rabbit heart with isoproterenol (ISOP). Bolus
injections of ISOP (475 pmol) produced a constant increase in
glycerol and 6-keto-PGF1[alpha] output. Infusion of sodium
meclofenamate (16 [mu]M) reduced basal and attenuated ISOP-induced 6
-keto-PGF1[alpha] output and enhanced glycerol output. During
inhibition of endogenous PG synthesis with meclofenamate, infusion of
PGI2 or PGE2 (0.1-1 [mu]M) inhibited ISOP-induced glycerol output.
Infusion of arachidonic acid (0.1-1 [mu]M) increased 6-keto
-PGF1[alpha] and reduced glycerol output. Infusion of sodium
meclofenamate abolished the effect of arachidonic acid to increase 6
-keto-PGF1[alpha] and to decrease glycerol output. These data suggest
that PGs synthesized in the heart act as an inhibitory modulator of
beta adrenergic receptor-stimulated cardiac lipolysis.
Received 26 December 1995; accepted in final form 6 May 1996.
APS Manuscript Number E595-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 June 96