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Ethanol Exposure Results in a Transient Decrease in Human Platelet cAMP Levels: Evidence for a Protein Kinase C Mediated Process
Author(s) -
DePetrillo P. B.,
Swift R. M.
Publication year - 1992
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1992.tb01379.x
Subject(s) - ibmx , protein kinase c , ethanol , phosphodiesterase , platelet , chemistry , protein kinase a , medicine , endocrinology , incubation , xanthine , phosphodiesterase inhibitor , phosphodiesterase 3 , kinase , enzyme , biochemistry , biology , in vitro , forskolin
At concentrations between 2 and 32 mM, ethanol is shown to depress human platelet cAMP levels. The effect is biphasic, maximal at 30 sec, with platelet concentrations of cAMP returning to baseline values at higher ethanol concentrations and at longer incubation times. The cAMP lowering effect of ethanol can be blocked by a phosphodiesterase (PPDE) inhibitor, 3‐isobutyl‐1‐methyl‐xanthine (IBMX), at a concentration of 2 mM, suggesting that an increase in PPDE activity may be responsible for this effect. Exposure of platelets to 1‐(5‐isoquinolinylsulfonyi)‐2‐methylpiperazine (H7), a protein kinase C (PKC) inhibitor, blocks the ethanol‐induced decrease in platelet cAMP, suggesting ethanol may be acting through activation of PKC.