Isolated rat adipocytes produce prostacyclin (PGI2) in relatively large quantities during norepinephrine (NE)-induced lipolysis. The endogenous NE-induced production rate of PGI2, calculated from the NE-induced production rate of PGI2 observed in our studies (2.2 ng/106 cells/2 h) and from the number of fat cells in the normal organism, is 1.46 ng/kg/min for rats, 4.46 ng/kg/min for men, and 11.86 ng/kg/min for women. These rates are comparable to the exogenous PGI2 infusion rate that alters platelet aggregation and blood pressure in rats and humans. Exogenous PGI2 failed to modify the rate of NE-induced lipolysis. Inhibition of endogenous PGI2 production by indomethacin had no effect on the rate of NE-induced lipolysis when either a maximal or submaximal lipolytic concentration of NE was used.

PGI2 [rather than prostaglandin (PG) E2] may be the substance that accounts for the functional vasodilatation that accompanies hormone-induced lipolysis. PGI2 is produced in larger quantities than PGE2 during NE-induced lipolysis and is a more potent vasodilator than PGE2. Its instability can account for the inability of previous investigators to detect a vasodilator substance in the venous effluent of adipose tissue.

The production of PGI2 by adipocytes may be an important modulator of the regulation of vascular tone and platelet aggregation by catecholamines in the vascular bed of adipose tissue and perhaps other tissues. PGI2 produced by adipocytes, by virtue of its ability to cause vasodilatation and inhibit platelet aggregation, may contribute to the maintenance of luminal patency in the vascular bed of adipose tissue and possibly other tissues as well.

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