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

  title={Modulation of beta-adrenergic receptor-stimulated lipolysis in the heart by prostaglandins.},
  author={Ying Ruan and Hong Kan and C Cano and Kafait U. Malik},
  journal={The American journal of physiology},
  volume={271 3 Pt 1},
  • Y. Ruan, H. Kan, +1 author K. Malik
  • Published 1 September 1996
  • Chemistry, Medicine
  • The American journal of physiology
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… Expand


Prostaglandins and the Release of the Adrenergic Transmitter
  • K. Malik, E. Sehic
  • Chemistry, Medicine
  • Annals of the New York Academy of Sciences
  • 1990
Observations and the findings that inhibitors of cyclooxygenase enhance NE release and the response of effector organs to nerve stimulation suggest that PGs act as physiological modulators of adrenergic transmission. Expand
Interaction of arachidonic acid metabolites and adrenergic nervous system.
  • K. Malik
  • Biology, Medicine
  • The American journal of the medical sciences
  • 1988
Prostaglandin synthesis elicited by alpha-1 adrenergic receptor activation in the kidney requires only partially extra- but mainly intracellular Ca++ and calmodulin, whereas PG synthesis in the heart is absolutely dependent upon extracellularCa++ but not on calmodoxin. Expand
Regulation by Calcium of Arachidonic Acid Metabolism in the Isolated Perfused Rabbit Heart
The data suggest that in the absence of perfusate Ca2+, the availability of exogenous arachidonic acid to cyclooxygenase is increased, possibly by reduced incorporation into tissue phospholipids. Expand
Role of prostaglandin-mediated cyclic AMP formation in protein kinase C-dependent secretion of atrial natriuretic peptide in rat cardiomyocytes.
Results suggest that PKC activation induces ANP secretion in spontaneously beating rat ventricular cardiomyocytes via an autocrine pathway involving increased PGI2 and/or PGE2 formation, a response leading to the activation of a myocardial adenylate cyclase and, subsequently, to that of a nifedipine-sensitive Ca2+ channel. Expand
Influence of prostacyclin on the antilipolytic effect of nicotinic acid in rat fat cells: a comparison with adenosine deaminase and theophylline.
The results indicate that the antilipolytic action of nicotinic acid is influenced by endogenous adenosine and is increased by PGI2, with a resulting decrease of the response to norepinephrine. Expand
Prostacyclin and lipolysis in rat fat cells.
The present results show that, under appropriate experimental conditions, PGI2 may act as a lipolytic agent in isolated fat cells and that some kind of interaction exists between stimulation of methylxanthine-sensitive adenosine receptors and stimulation of P GI2 receptors. Expand
Effect of prostaglandins on guinea pig myocardial adenyl cyclase.
The data suggests that there are separate receptors on one adenyl cyclase in the guinea pig heart, one responsive to prostaglandins the other to norepinephrine. Expand
Investigations on the mechanism of the prostaglandin E1 antagonism to norepinephrine and theophylline-induced lipolysis
Abstract The effects of prostaglandin E1 (PGE1) on the dose-response curves of glycerol release from adipose tissue by norepinephrine and theophylline have been investigated in vitro. PGE1Expand
Indomethacin, lipolysis, and cyclic AMP accumulation in white fat cells.
Results indicate that indomethacin (5 to 50 μg/ml) has little, if any, effect on lipolysis and suggest that prostaglandins are not important feedback regulators of adenylate cyclase orlipolysis in isola... Expand
Enhanced prostaglandin synthesis due to phospholipid breakdown in ischemic-reperfused myocardium. Control of its production by a phospholipase inhibitor or free radical scavengers.
The results suggest that the arachidonate cascade is activated during reperfusion of ischemic myocardium as a consequence ofospholipid breakdown, and this activation can be attenuated by inhibiting phospholipases or enhanced by scavenging oxygen-free radicals generated during reperFusion. Expand