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PubMed1977

Collagen-mediated platelet aggregation. Evidence for multivalent interactions of intermediate specificity between collagen and platelets.

We have shown previously that periodate oxidation of collagen carbohydrate does not affect its ability to aggregate platelets. We now describe an additional characterization of periodate-modified collagen which demonstrates that collagen devoid of intact carbohydrate is fully capable of fibril formation, and we confirm its capacity to initiate platelet aggregation. Furthermore, we demonstrate that the platelet aggregating abilities of Types I, II, and III fibrillar collagen are quite similar despite differences in carbohydrate content and amino acid sequence. We also demonstrate that monomeric, pepsin-solubilized Type I human collagen is ineffective inhibiting aggregation by performed fibrils derived from the same molecule, thus establishing that the affinity of platelets for collagen depends upon prior polymerization of collagen. We interpret these and other findings to demonstrate that the hydroxylysyl glycoside regions of collagen are not highly specific sites involved in platelet-collagen interactions leading to "physiological" aggregation, and that the possibility must be considered that multiple interactions involving collagen sites of comparatively low structural specificity may be the initiating events in release of platelet ADP and the ensuing aggregation.

Amino Acids↗
PubMed1985

Zinc-induced platelet aggregation is mediated by the fibrinogen receptor and is not accompanied by release or by thromboxane synthesis.

We demonstrate that zinc (0.1 to 0.3 mmol/L) induces aggregation of washed platelet suspensions. Higher concentrations (1 to 3 mmol/L) of zinc were needed to aggregate platelets in platelet-rich plasma obtained from blood anticoagulated with low-molecular-weight heparin, probably due to the binding of zinc to the plasma proteins. Zinc-induced aggregation of normal washed platelets required added fibrinogen and no aggregation occurred with thrombasthenic platelets or with normal platelets pretreated with a monoclonal antibody (10E5) that blocks the platelet fibrinogen receptor. These data indicate that the platelet membrane fibrinogen receptor-glycoproteins IIb and IIIa mediate the effect of zinc. Zinc-induced aggregation was blocked by the agent TMB-8, which interferes with the internal calcium flux, and by prostacyclin, which elevates platelet cyclic adenosine monophosphate levels. Zinc-induced aggregation was not accompanied by thromboxane synthesis or by the secretion of dense-body serotonin and was not affected by preexposure of platelets to acetylsalicylic acid. Experiments with creatine phosphate/creatine phosphokinase showed that the zinc effect on platelets was independent of extracellular adenosine diphosphate (ADP). Zinc had an additive effect when platelet aggregation was stimulated with subthreshhold concentrations of collagen or ADP. Together with the known effects of nutritional zinc on in vivo bleeding, on platelet aggregation, and on lipid metabolism, the results suggest that zinc may have an important bearing on normal hemostasis, thrombosis, and atherosclerosis.

Adenosine Diphosphate↗
PubMed1996

Studies on tumor-cell-induced platelet aggregation in human lung cancer cell lines.

We investigated the ability of human lung cancer cells of different histological subtypes to cause platelet aggregation. Tumor-cell-induced platelet aggregation (TCIPA) was studied in vitro in 13 human lung cancer cell lines [small-cell lung cancer (SCLC), squamous-cell lung cancer, large-cell lung cancer, adenocarcinoma and alveolar-cell lung cancer]. Three tumor cell lines failed to aggregate platelets in platelet-rich plasma, whereas platelet aggregation was induced by 12 cell lines when added to washed platelets and minimal amounts of platelet-poor plasma (0.5% v/v). The thrombin antagonist hirudin inhibited TCIPA in non-small-cell lung cancer cell lines (NSCLC). In SCLC, TCIPA was fully abolished only when the ADP scavenger apyrase was added to hirudin. Thus ADP and thrombin generation by these tumor cell lines are responsible for platelet aggregation. The ability to activate platelets independently of coagulation factors VII and X was demonstrated for 8 cell lines. Electron-microscopically, direct tumor-cell/platelet contact was found to be the initiating mechanism of TCIPA in SCLC, whereas tumor-cell/platelet contacts in NSCLC could only be observed at the peak of the aggregation curve. Lung cancer cells activate platelets in vitro by generation of thrombin and/or ADP.

Blood Platelets↗
PubMed1987

Circulating aggregated platelets in coronary artery disease.

Circulating aggregated platelets were assessed in 30 patients with stable angina, 22 with unstable angina and 50 with acute myocardial infarction (AMI). Fifty healthy volunteers and 20 noncardiac patients served as controls. One milliliter of venous blood was separated into 2 solutions: 1 composed of ethylenediamine tetraacetic acid (EDTA) and formalin containing reversible and aggregates and 1 composed of EDTA alone containing irreversible aggregates only. By direct microscopic readings the percentage of platelets forming aggregates/1,000 counted platelets was determined in the 2 solutions. The number of reversibly aggregated platelets was estimated by subtracting the percentage of aggregated platelets in the second solution from that in the first solution. In patients with stable angina the percentage of aggregated platelets was higher than in control subjects (15 +/- 4% vs 7 +/- 2%, p less than 0.001). Most aggregated platelets (72% and 76%, respectively) were irreversibly aggregated. In the unstable angina group the percentage of aggregated platelets was similar to that of the AMI group (24 +/- 13% and 24 +/- 10%) and significantly higher than in the stable angina group. Only 11% and 17% of aggregated platelets in patients with stable angina and AMI were irreversibly aggregated and 89% and 83% of them were reversibly aggregated. Participation of platelets in the pathogenesis of unstable angina and AMI may be related to the early reversible phase of platelet activation.

Angina Pectoris↗
PubMed1998

Concomitant activation of Gi and Gq protein-coupled receptors does not require an increase in cytosolic calcium for platelet aggregation.

U46619 is a potent platelet agonist, its binding to the thromboxane A2 receptor resulting in Gq-binding protein-mediated responses; nevertheless, it is unable to cause platelet aggregation, unless released ADP is present. In this study we demonstrate that Gi activation is the step U46619 lacks to cause platelet aggregation; in fact, when platelets were treated with an ADP scavenger system, the response to U46619 was restored by the addition of epinephrine, which activates platelets via a Gi protein. The concomitant activation of Gi and Gq proteins does not require increased cytosolic calcium to cause aggregation, as assessed by the fact that platelets treated with the intracellular calcium chelator BAPTA were able to respond to U46619 provided ADP or epinephrine was present. Moreover, as the calcium ionophore ionomycin, at low concentrations, potentiated the response to U46619 but not to epinephrine, we may conclude that calcium influx preferentially activates a Gi downstream signalling pathway.

Adenosine Diphosphate↗
PubMed1987

Mechanisms of platelet aggregation by viridans group streptococci.

The direct aggregation of platelets is thought to be an important event in the pathogenesis of viridans streptococcal endocarditis, but the mechanisms for platelet activation are unknown. We evaluated the processes by which two endocarditis-producing strains of viridans group streptococci activated human platelets in vitro, as measured by platelet cyclooxygenase activity, secretion, and aggregation. Addition of either streptococcal strain to platelets suspended in whole plasma resulted in a mean lag phase of 15.3 min, followed by platelet secretion and brisk aggregation. The lag phase duration was dependent on the platelet donor and appeared to be a function of direct platelet-bacterial interaction. Aggregation was partially inhibited by 20 muM [corrected] indomethacin and blocked completely by 1 mg of apyrase, an extracellular ADP hydrolase, per ml. Neither strain aggregated washed platelets suspended in Tyrode solution alone. However, both strains produced maximal aggregation when the platelet suspension was supplemented with 10% (final concentration) normal plasma. Studies with factor-deficient plasmas demonstrated that exogenous fibrinogen was required for aggregation. One or more additional plasma components were needed, which eluted with a molecular weight of 67,000 to 130,000 on gel permeation chromatography. These cofactors have not been described for other platelet agonists, which suggests that viridans streptococci may aggregate human platelets by a novel mechanism.

Adenosine Diphosphate↗
PubMed2001

Evidence for cross-talk between glycoprotein VI and Gi-coupled receptors during collagen-induced platelet aggregation.

Collagen-induced platelet aggregation is a complex process and involves synergistic action of integrins, immunoglobulin (Ig)-like receptors, G-protein-coupled receptors and their ligands, most importantly collagen itself, thromboxane A(2) (TXA(2)), and adenosine diphosphate (ADP). The precise role of each of these receptor systems in the overall processes of activation and aggregation, however, is still poorly defined. Among the collagen receptors expressed on platelets, glycoprotein (GP) VI has been identified to play a crucial role in collagen-induced activation. GPVI is associated with the FcRgamma chain, which serves as the signal transducing unit of the receptor complex. It is well known that clustering of GPVI by highly specific agonists results in platelet activation and irreversible aggregation, but it is unclear whether collagen has the same effect on the receptor. This study shows that platelets from Galphaq-deficient mice, despite their severely impaired response to collagen, normally aggregate on clustering of GPVI, suggesting this not to be the principal mechanism by which collagen activates platelets. On the other hand, dimerization of GPVI by a monoclonal antibody (JAQ1), which by itself did not induce aggregation, provided a sufficient stimulus to potentiate platelet responses to Gi-coupled, but not Gq-coupled, agonists. The combination of JAQ1 and adrenaline or ADP, but not serotonin, resulted in alpha(IIb)beta(3)-dependent aggregation that occurred without intracellular calcium mobilization and shape change in the absence of Galphaq or the P2Y(1) receptor. Together, these results provide evidence for a cross-talk between (dimerized) GPVI and Gi-coupled receptors during collagen-induced platelet aggregation. (Blood. 2001;97:3829-3835)

Animals↗
PubMed1981

Pathophysiological aspects of platelet aggregation in relation to blood flow rheology in microcirculation.

Platelet aggregates play an important role in rheology of the blood flow in microcirculation. The formation of platelet aggregates markedly raise the threshold diameter of the vessel at which the inversion of Fahraeus-Lindquist effect takes place. In different diseases (ischemic heart disease, diabetes) thromboxane A2 production by platelets is increased and, as a consequence, platelet aggregate formation is facilitated. Platelet aggregation is modulated by several mechanisms, among which thromboxane A2 and thrombin increase and prostacyclin decrease formation of platelet aggregates. Prostacyclin is able also to increase blood red cells deformability thus it appears one of the most important factors for the control of blood flow rheology in microcirculation. However, prostacyclin production is limited in time, and repeated and close periods of venous stasis induce exhaustion of prostacyclin production and increase the formation of platelet aggregates.

Adenosine Diphosphate↗
PubMed1998

[Method of quantitative measurement of human platelet aggregation in clinical practice].

We examined the quantitative measurement of platelet aggregation in 20 volunteers and 89 patients with ischemic heart disease (IHD). Subjects in whom platelet aggregation was induced by an adenosine diphosphate (ADP and an epinephrine solution were clearly divided into two groups: "normal" and "accentuated". We chose the maximum aggregation time for the ADP solution and the maximum transmission rate for the epinephrine solution for the quantitative measurement of platelet aggregation. The results were as follows. The maximum aggregation time with a 1.0 microM ADP solution in the normal group of 13 volunteers was 0.71 +/- 0.12 min, (mean +/- SD), in 50 IHD patients it was 0.91 +/- 0.49 min, in the "accentuated" group of 7 volunteers it was 5.34 +/- 1.18 min, in 39 IHD patients it was 6.01 +/- 1.22 min. The maximum light transmission rate with a 0.1 microM epinephrine solution in the normal group of 14 volunteers was 8.04 +/- 4.14%, in 52 IHD patients it was 13.74 +/- 5.75%, in the "accentuated" group of 6 volunteers it was 76.33 +/- 9.91%, and in 37 IHD patients it was 77.26 +/- 13.39%. The difference between the "normal" and "accentuated" groups was statistically significant (p < 0.001), with the ADP and with the epinephrine solution. Next, we examine the effect of antiplatelet therapy (dipyridamole and aspirin) on 15 patients selected from among those with IHD who had accentuated platelet aggregation when the ADP solution was added. Their maximum aggregation time was 5.98 +/- 1.24 min, and their maximum platelet aggregation rate when the epinephrine solution was added was 78.90 +/- 11.60% (10 patients), 20.00 +/- 3.24% (5 patients). After the therapies, the maximum aggregation time in 10 patients was 0.94 +/- 0.21 min (return to normal condition), and in 5 patients it was 5.90 +/- 1.09 min (not effective). The maximum platelet aggregation rate in 10 patients was 14.11 +/- 5.88% (normal condition), and in 5 patients it was 75.00 +/- 9.51% (not effective). Finally, we examined the long term effects of various antiplatelet drugs. Most of the patients in whom platelet aggregation was accentuated got well.

Adenosine Diphosphate↗
PubMed2001

Enhanced platelet aggregation in the coronary circulation after coronary spasm.

A recently developed platelet aggregometer using a laser light scattering method is capable of monitoring the increase in size of small-sized platelet aggregates (diameter 9-25 microm), which cannot be detected with the conventional methods. Whether coronary spasm can cause platelet aggregation in the coronary circulation is unknown. We investigated platelet aggregation, especially small-sized platelet aggregates, simultaneously in the coronary sinus and the aortic root in 18 patients with coronary spastic angina before and after a left coronary artery spasm induced by intracoronary injection of acetylcholine, and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid right atrial pacing. Platelet aggregation in 12 patients with chest pain syndrome was also examined before and after coronary spasms provoked by acetylcholine. The number of small-sized platelet aggregates increased significantly in the coronary sinus [2.0+/-0.6 x 104 to 4.1+/-1.0 x 104 (V), P<.01] and in the aortic root [1.7+/-0.6 x 104 to 3.2+/-0.6 x 104 (V), P<.05], and the coronary sinus-arterial difference in the number of small-sized platelet aggregates [2.3+/-1.9 x 103 to 1.1+/-0.4 x 104 (V), P<.01] increased significantly after attacks in the coronary spastic angina group, but remained the same in the stable exertional angina group after attacks and in the chest pain syndrome group after the administration of acetylcholine. Therefore, we can conclude that acute myocardial ischemia induced by coronary spasm causes platelet aggregation in the coronary circulation.

Acetylcholine↗
PubMedDate not supplied

The relationship between carotid atherosclerosis and platelet aggregation in elderly.

The aim of this study is to assess the relationship between the carotid wall intima media thickness (IMT) and atheroma plaques due to atherosclerosis and platelet aggregation among elderly. The first stage of the study was performed by analyzing platelet aggregation in a total of 28 elderly patients divided into two groups. The first group consisted of 14 cases with carotid atheroma plaque (Patient group I) and the second group of patients were without carotid atheroma plaque (Control group I). At the second stage of the study, the cases were regrouped according to the carotid IMT. Patients with IMT above 1 mm (Patient group II, n=10) and under 1 mm (Control group II, n=14) were compared regarding platelet aggregation. Platelet aggregation was induced in the platelet-rich plasma using 5 micro M ADP, 0.2 mg/ml collagen and 1.2 mg/ml ristocetin. Between patients with and without atheroma, no difference was noted in terms of platelet aggregation. Between platelet aggregation results of patients with intimal thickness above and under 1 mm, no significant difference was also noted. Between elderly cases with or without atherosclerosis, there was no difference with respect to platelet aggregation. Platelet aggregation measurements cannot be used as a marker of atherosclerosis in elderly population.

Aged↗
PubMed1995

Daily variation of serum lipids in relation to the circadian rhythm of platelet aggregation in healthy male persons.

The circadian rhythm of platelet aggregation was compared with that of serum lipids in seven healthy male persons. Daily variations of remnant lipoprotein-cholesterol and of remnant lipoprotein-triglycerides were related to those of arachidonic acid-, ADP (adenosine diphosphate)-, and collagen-induced aggregation in platelet-rich plasma and to ADP-induced aggregation in whole blood, respectively. Statistical analyses indicate that the time course of remnant-cholesterol was correlated to that of ADP-induced aggregation in platelet-rich plasma and the time courses of blood cholesterol and triglyceride were correlated to arachidonic acid- and serotonin-induced platelet aggregation in platelet-rich plasma, respectively. In whole blood, the time course of remnant lipoprotein-triglyceride was correlated only to ADP-induced platelet aggregation. In contrast, the daily variation of HDL (high density lipoprotein)-cholesterol did not influence either that of platelet aggregation in platelet-rich plasma or that in whole blood. Our findings are of clinical interest regarding the development of atherosclerosis and thrombotic events in persons with an elevated level of serum lipids.

Adolescent↗
PubMed1999

cAMP is an important messenger for ADP-induced platelet aggregation.

In rat platelets, basal cAMP levels were not changed upon stimulation with ADP and it was concluded that cAMP is not an important messenger for ADP-induced aggregation (Savi et al., Blood Coagul Fibrinolysis, 1996; 7: 249-52). In the present study, the effects of prostaglandin E(1) (PGE(1)) and ADP on human platelet aggregation, cAMP generation and VASP phosphorylation were studied. Phosphorylation of the protein kinase A (PKA) substrate VASP and inhibition of platelet aggregation by PGE(1) occurred without measurable changes in cellular cAMP levels. In addition, a marked inhibition of basal VASP phosphorylation by ADP was observed. It is concluded that cAMP determinations do not necessarily detect a possible activation or inhibition of the cAMPPKA pathway in platelets. Thus, cAMP might well be an important second messenger for ADP-induced platelet aggregation.

Journal Article↗
PubMed1991

Effects of prostaglandins, cAMP, and changes in cytosolic calcium on platelet aggregation induced by a thromboxane A2 mimic (U46619).

The effects of U46619, a thromboxane mimic, on cytosolic Ca2+ concentration and platelet aggregation were determined in human platelets. Cytosolic Ca2+ concentration was determined by Quin-2 fluorescence and platelet aggregation quantitated with an aggregometer. Addition of U46619 (1 x 10(-7) M) to the platelet suspension produced a rapid increase in cytosolic Ca2+ and platelet aggregation. Pretreatment of platelets with EGTA (3 x 10(-3) M), verapamil (5 x 10(-4) M), a calcium entry blocker, or 8-(diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride (1 x 10(-3) M), an inhibitor of intracellular Ca2+ release, either blunted or markedly delayed the rate, but not the magnitude, of increase in cytosolic Ca2+ and prevented platelet aggregation by U46619. Pretreatment of platelets with prostaglandin I2 (PGI2) (5 x 10(-8) M), PGD2 (5 x 10(-8) M), PGE1 (5 x 10(-8) M), PGF2 alpha (1 x 10(-5) M), dibutyryl cAMP (5 x 10(-3) M), or forskolin (1 x 10(-6) M) prevented both the increase in cytosolic Ca2+ and the associated platelet aggregation induced by U46619. These data suggest that U46619 may induce platelet aggregation through an increase in cytosolic Ca2+, and that both Ca2+ entry and its release from intracellular storage sites probably contribute to the increase in cytosolic Ca2+. Furthermore, the rate of the increase in cytosolic Ca2+ concentration, as well as the magnitude of the increase, appear to be critical for platelet aggregation induced by U46619. Our data are consistent with the hypothesis that PGs inhibit U46619-induced platelet aggregation by preventing the increase in cytosolic Ca2+, and that these effects may be mediated via an increase in cAMP, since they were induced by PGs and cAMP.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Human laminin produces human platelet aggregation in vitro.

The effects of laminin isoforms on platelet aggregation were compared and characterized in platelet rich plasma (PRP) obtained from 26 healthy human volunteers. In approximately 38% of the individuals tested, human laminin produced a biphasic platelet aggregation response. Human laminin produced only a primary phase in the remaining "non-responsive" individuals. Mouse laminin, rat laminin and human merosin did not cause platelet aggregation in any of the volunteers. The biphasic platelet aggregation response caused by human laminin was concentration-dependent (0.3-30 nM) and was consistently observed upon repeated testing of "responsive" individuals. The secondary phase of aggregation produced by human laminin in "responsive" individuals was abolished by aspirin, SQ 29,548, a selective thromboxane antagonist, and SK&F 106760, an RGD-derived platelet fibrinogen receptor (GPIIb/IIIa) antagonist. Also, the secondary phase of aggregation was not observed in washed platelets. Both the primary and secondary platelet responses produced by human laminin were abolished by a VLA-6 (alpha 6 beta 1) monoclonal antibody, but not by the YIGSR pentapeptide. In conclusion, human laminin causes thromboxane-dependent platelet aggregation, in vitro, in a significant population of human volunteers. The aggregation response was dependent upon the interaction of human laminin with platelet VLA-6 (alpha 6 beta 1). These novel results suggest that in some individuals laminin may play an important role in hemostasis and thrombogenesis.

Adult↗
PubMed1993

Collagen induced human platelet aggregation: serotonin receptor antagonism retards aggregate growth in vitro.

OBJECTIVE: The role of platelet derived serotonin (5-HT) in collagen induced human platelet aggregation was examined both in hirudinised plasma and whole blood. Hirudin was used to maintain normocalcaemia, thereby avoiding erroneous findings often obtained with citrated blood. METHODS: Platelet aggregation, aggregate growth, and primary platelet aggregation were quantified by optical aggregometry and platelet counting respectively. RESULTS: In plasma, platelet aggregation induced by 5-HT (3 microM) in the presence of adrenaline (1 microM) was inhibited by more than 85% by ICI 170809 (3 microM, IC50 0.1 microM), a specific platelet 5-HT2 antagonist. With collagen (0.5 micrograms.ml-1), ICI 170809 retarded the rate of aggregation by 30%, whereas aspirin abolished the response. In contrast, ICI 170809 inhibited collagen induced primary aggregation by less than 10% in both plasma and whole blood. CONCLUSIONS: (1) 5-HT contributes to collagen induced aggregate growth and 5-HT2 receptor antagonism with ICI 170809 retards the rate of growth. (2) This could explain the efficacy of 5-HT2 antagonists in limiting coronary thrombosis despite the limited role of 5-HT in primary aggregation.

Apyrase↗
PubMed1983

Inhibition of fibrinogen receptor-mediated platelet aggregation by heterologous anti-human platelet membrane antibody. Significance of an Mr = 66,000 protein derived from glycoprotein IIIa.

Heterologous anti-human platelet membrane antisera were raised in rabbits against membranes prepared from human intact or chymotrypsin- or pronase-treated platelets. Anti-intact, anti-chymotrypsin, and anti-pronase-treated platelet membrane antibodies (IgG and Fab fragments) inhibited the fibrinogen-induced aggregation of ADP-stimulated platelets and of chymotrypsin-treated platelets. The specific binding of 125I-fibrinogen to these platelets was also inhibited. As revealed by the sodium dodecyl sulfate-polyacrylamide gel electrophoresis of 125I-surface-radiolabeled platelet proteins and by the electrophoresis of the immunoprecipitates prepared from these labeled proteins, predominant components on the surface of intact platelets were glycoproteins IIb and IIIa. These proteins were immunoprecipitated by all three antibodies. In addition, chymotrypsin-treated platelets contained an Mr = 66,000 protein on their surface that was also immunoprecipitated by the three types of anti-platelet membrane antibodies. The appearance of this Mr = 66,000 protein on the surface of chymotrypsin-treated platelets correlated with the exposure of fibrinogen receptors on the platelet surface as evidenced by the increased platelet aggregation and the enhanced 125I-fibrinogen binding shown by chymotrypsin-treated platelets. The origin of the Mr = 66,000 protein labeled on chymotrypsin-treated platelets was studied by first labeling intact platelets with 125I and then treating these platelets with chymotrypsin. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the total labeled proteins present after chymotrypsin treatment and those immunoprecipitated by anti-pronase-treated platelet membrane antibody from detergent extracts of chymotrypsin-treated platelets suggested that the Mr = 66,000 protein was a proteolytic cleavage product of glycoprotein IIIa. Analysis on sodium dodecyl sulfate gels of the major chymotryptic cleavage products of partially purified glycoprotein IIIa and analysis of the peptide of glycoprotein IIIa immunoprecipitated by anti-pronase-treated platelet membrane antibody revealed that the Mr = 66,000 protein produced by chymotrypsin on the platelet surface was the major chymotryptic cleavage product of glycoprotein IIIa. We propose a hypothesis that the Mr = 66,000 is a part of glycoprotein IIIa present on the surface of proteolytically treated platelets and it may function in fibrinogen binding and fibrinogen-induced platelet aggregation and that the 66,000-dalton region of glycoprotein IIIa in intact platelets may represent the fibrinogen-binding domain of glycoprotein IIIa.

Adenosine Diphosphate↗
PubMed1983

Role of activated protein C on platelet aggregation induced by thrombin.

Platelets aggregate with thrombin-free activated protein C in concentrations higher than physiological levels. Aggregation was dependent on an intact release mechanism since inhibition of aggregation occurred with adenosine or EDTA. However, activated protein C reduced the sensitivity of platelets to aggregate in the presence of thrombin. Probably, activated protein C competes for membrane sites sensitive to thrombin.

Adenosine↗