Prostaglandin Deficiency Promotes Sensitization of Adenylyl Cyclase
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Abstract
Inhibition of prostaglandin synthesis by the drug indomethacin suppresses the synthesis of the cyclic AMP antagonist, prostaglandylinositol cyclic phosphate (cyclic PIP), and leads to a metabolic state comparable to type II diabetes. It was of interest whether prostaglandindeficiency likewise causes sensitization of adenylyl cyclase, as this has been reported for the diabetic state. In liver plasma membranes of indomethacintreated male rats, basal and forskolinstimulated cyclic AMP synthesis remained unchanged when compared to untreated control rats. In control rats, stimulation of cyclic AMP synthesis by fluoride (2.2-fold) or glucagon (3.5-fold) was much lower than stimulation by forskolin (6.6-fold). In contrast, in indomethacin treated rats, stimulation of cAMP synthesis by fluoride (4.6-fold) or glucagon (5.2-fold) nearly matched the stimulation by forskolin (6.4-fold). The level of α[1]adrenergic receptors was slightly reduced, from 450 to 320 fmol/mg protein, by the indomethacin treatment. Independent of the treatment by indomethacin, stimulation of cyclic AMP synthesis by adrenaline failed, in agreement with the low density of adrenergic βreceptors. In conclusion, PGE deficiency sensitizes adenylyl cyclase in rat liver for G proteincoupled receptors (glucagon) and also for fluoride.
Copyright © 2000 by Walter de Gruyter GmbH & Co. KG
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- Regulation of GTPases in the Bacterial Translation Machinery
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- The Role of Heterotrimeric G Proteins in Platelet Activation
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