EFFECTS OF C-REACTIVE PROTEIN ON PLATELET-FUNCTION .3. ROLE OF CAMP, CONTRACTILE ELEMENTS, AND PROSTAGLANDIN METABOLISM IN CRP-INDUCED INHIBITION OF PLATELET-AGGREGATION AND SECRETION

Google Scholar
  • 1 January 1977
    • journal article
    • research article
    • Vol. 119  (3) , 877-882
Abstract
Multiple considerations including selective inhibition of secondary wave aggregation suggested that CRP [C-reactive protein] exerted its inhibitory effects by interfering with the release of endogenous ADP. CRP was found by direct assay to inhibit the release of endogenous ADP and/or serotonin concomitant with inhibition of platelet [human] aggregation stimulated by ADP, epinephrine, thrombin and AHGG [aggregated human .gamma. globulin]. CRP did not induce an increase in the basal level of platelet c[cyclic]AMP, suggesting independence of a direct effect upon this mediator system. CRP did not inhibit the aggregation and secretion induced by the antibiotic ionophore A23187, suggesting the absence of a direct effect upon the activation of platelet contractile elements. By contrast, CRP did inhibit both thrombin-induced release of malondialdehyde, a prostaglandin endoperoxide nonprostanoate endproduct, and platelet aggregation induced by the prostaglandin endoperoxide precursor arachidonic acid. CRP may inhibit platelet reactivities by interfering with an aspect of prostaglandin metabolism, and this apparently occurs subsequent to the hydrolytic accumulation of arachidonic acid and prior to the movement of Ca from the platelet dense tubules. These studies support the concept that CRP serves to modulate platelet reactivities during acute inflammatory reactions.