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Alpha‐Adrenergic Stimulation of Phosphatidylinositol Synthesis in Human Platelets as an Alpha‐2 Effect Secondary to Platelet Aggregation
Author(s) -
Wallace Michael A.,
Agarwal Kailash C.,
GarciaSainz J. Adolfo,
Fain John N.
Publication year - 1982
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.1982.240180208
Subject(s) - phosphatidylinositol , yohimbine , prazosin , epinephrine , chemistry , platelet , endocrinology , medicine , stimulation , antagonist , alpha (finance) , agonist , alpha 2 adrenergic receptor , adrenergic receptor , adenosine diphosphate , pharmacology , biochemistry , platelet aggregation , receptor , phosphorylation , construct validity , nursing , patient satisfaction
Epinephrine and adenosine diphosphate (ADP) stimulated 3 H‐glycerol uptake into phosphatidylinositol of human platelets. Yohimbine, an alpha‐2 adrenoceptor antagonist, markedly reduced epinephrine‐stimulated 3 H‐glycerol uptake into phosphatidylinositol; while prazosin, an alpha‐1 antagonist, was without effect. Likewise, yohimbine, but not prazosin, blocked epinephrine‐induced platelet aggregation. Furthermore, clonidine, a specific agonist for alpha‐2 adrenoceptors, stimulated incorporation of‐ 3 H‐glycerol into phosphatidylinositol and promoted platelet aggregation in the presence of low concentrations of ADP. These studies indicate that the effects of epinephrine on platelet aggregation and phosphatidylinositol synthesis are mediated through alpha‐2 adrenoceptors. Further, since the stimulation of phosphatidylinositol synthesis seen with epinephrine was also observed with ADP, this suggests that the increased 3 H‐glycerol labeling is an indirect result of platelet aggregation.