Y. Ruan et al., MODULATION OF BETA-ADRENERGIC RECEPTOR-STIMULATED LIPOLYSIS IN THE HEART BY PROSTAGLANDINS, American journal of physiology: endocrinology and metabolism, 34(3), 1996, pp. 556-562
The purpose of the present study was to investigate the contribution o
f prostaglandins to lipolysis elicited by beta-adrenergic receptor act
ivation in the heart. We have studied the effect of prostaglandin E(2)
(PGE(2)), prostaglandin I-2 (PGI(2)), and their precursor arachidonic
acid (AA) in the presence and absence of a cyclooxygenase inhibitor,
sodium meclofenamate, on glycerol output elicited by stimulation of be
ta-adrenergic receptors in the isolated rabbit heart with isoprotereno
l (ISOP). Bolus injections of ISOP (475 pmol) produced a constant incr
ease in glycerol and 6-ketoprostaglandin F-1 alpha (6-keto-PGF(1 alpha
)) output. Infusion of sodium meclofenamate (16 mu M) reduced basal an
d attenuated ISOP-induced 6-keto-PGF(1 alpha) output and enhanced glyc
erol output. During inhibition of endogenous prostaglandin synthesis w
ith meclofenamate, infusion of PGI(2) or PGE(2) (0.1-1 mu M) inhibited
ISOP-induced glycerol output. Infusion of AA (0.1-1 mu M) increased 6
-keto-PGF(1 alpha) and reduced glycerol output. Infusion of sodium mec
lofenamate abolished the effect of AA to increase 6-keto-PGF(1 alpha)
and to decrease glycerol output. These data suggest that prostaglandin
s synthesized in the heart act as an inhibitory modulator of p-adrener
gic receptor-stimulated cardiac lipolysis.