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Regulation of platelet cytosolic free calcium by cyclic nucleotides and protein kinase C
Author(s) -
MacIntyre D.E.,
Bushfield M.,
Shaw A.M.
Publication year - 1985
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(85)80407-5
Subject(s) - second messenger system , chemistry , protein kinase c , cyclase , diacylglycerol kinase , platelet , adenylate kinase , protein kinase a , endocrinology , medicine , cytosol , cyclic nucleotide , phorbol , sodium nitroprusside , calcium , biochemistry , nucleotide , kinase , signal transduction , receptor , enzyme , biology , nitric oxide , organic chemistry , gene
PAF elicits a rapid, concentration‐dependent elevation of platelet cytosolic free calcium ([Ca f ]), measured by quin2. Elevation of [Ca f ] is transient, and the rate of reversal increases with agonist concentration. Adenylate cyclase stimulants (PGI 2 , PGD 2 ) and 8‐bromo cAMP; a guanylate cyclase stimulant (sodium nitroprusside) and 8‐bromo cGMP; and a protein kinase C stimulant (phorbol myristate acetate) block the elevation of [Ca f ] induced by PAF, and accelerate its reversal. These results suggest that cAMP, cGMP and 1,2‐diacylglycerol (DAG) could act as second messengers to regulate [Ca f ] in platelets. As PAF is known to stimulate platelet phosphoinositide hydrolysis (ergo DAG formation) but fails to elevate platelet cAMP or cGMP, it is proposed that DAG, via activation of protein kinase C, may act as an endogenous modulator of platelet [Ca f ]: an action that contributes to the role of DAG as a bi‐directional regulator of platelet reactivity.