Influence of prostacyclin on the antilipolytic effect of nicotinic acid in rat fat cells: A comparison with adenosine deaminase and theophylline

The purpose of the present study was to investigate the contribution of prostaglandins to lipolysis elicited by beta-adrenergic receptor activation in the heart. We have studied the effect of prostaglandin E2 (PGE2), prostaglandin I2 (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-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) output. Infusion of sodium meclofenamate (16 microM) reduced basal and attenuated ISOP-induced 6-keto-PGF1 alpha output and enhanced glycerol output. During inhibition of endogenous prostaglandin synthesis with meclofenamate, infusion of PGI2 or PGE2 (0.1-1 microM) inhibited ISOP-induced glycerol output. Infusion of AA (0.1-1 microM) increased 6-keto-PGF1 alpha and reduced glycerol output. Infusion of sodium meclofenamate abolished the effect of AA to increase 6-keto-PGF1 alpha and to decrease glycerol output. These data suggest that prostaglandins synthesized in the heart act as an inhibitory modulator of beta-adrenergic receptor-stimulated cardiac lipolysis.

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Modulation of beta-adrenergic receptor-stimulated lipolysis in the heart by prostaglandins

Ruan

Kan

Cano

et al. 1996

American Journal of Physiology-Endocrinology and Metabolism

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Influence of prostacyclin on the antilipolytic effect of nicotinic acid in rat fat cells: A comparison with adenosine deaminase and theophylline

Cited by 1 publication

References 12 publications

Modulation of beta-adrenergic receptor-stimulated lipolysis in the heart by prostaglandins

Modulation of beta-adrenergic receptor-stimulated lipolysis in the heart by prostaglandins

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