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

Isolated rat fat cells were incubated at pH 8.5 in order to delay PGI2 inactivation. Nicotinic acid, at concentrations lower than 2 mM was ineffective in antagonizing the stimulation of lipolysis induced by norepinephrine (2 microM). The potentiation of norepinephrine effect due to PGI2 (0.1 microM) was abolished by 0.1 mM nicotinic acid and, at higher concentrations of the drug, the rate of the process fell below the one measured in the absence of PGI2, with a resulting decrease of the response to norepinephrine. Nicotinic acid (0.04-0.4 mM) antagonized the stimulation of lipolysis caused by adenosine deaminase (0.5 U/ml) or by theophylline (0.5 mM) and the potentiation of norepinephrine effect due to adenosine deaminase. In cells treated with adenosine deaminase (0.5 U/ml) or with theophylline (0.5 mM), PGI2 (40 nM) inhibited the lipolytic effect of norepinephrine (5 microM) and nicotinic acid acted synergistically with PGI2 at this level. These results indicate that the antilipolytic action of nicotinic acid is influenced by endogenous adenosine and is increased by PGI2.