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PubMed1994

Platelet-activating factor (PAF)-induced platelet aggregation. Modulation by plasma adenosine and methylxanthines.

This study examined the role of plasma adenosine in the modulation of platelet-activating factor (PAF) activity on platelet aggregation and serotonin (5-HT) release in human platelet-rich plasma (PRP). In addition, the effects of methylxanthines (e.g. theophylline and caffeine) were studied on PAF-induced platelet aggregation in PRP isolated from blood samples from healthy subjects. Also, PAF-induced platelet aggregation was examined in PRP samples of patients receiving theophylline treatment. These studies demonstrate that plasma adenosine levels (0.1 to 0.3 microM) play a key role in negative modulation of PAF activity on platelet aggregation and 5-HT release. After depletion of plasma adenosine, the platelet-aggregating activity of PAF was increased greatly (> 10-fold). PAF at concentrations of 0.1 to 12 microM caused no 5-HT release in PRP containing normal amounts of adenosine (blood collected in the presence of 2'-deoxycoformycin and dilazep), whereas PAF at 0.1 microM caused 5-HT release (45%) in adenosine-depleted PRP, demonstrating that plasma adenosine is much more inhibitory of 5-HT release than platelet aggregation. The adenosine antagonists theophylline (50 microM), caffeine (50 microM) and a xanthine derivative, 3,7-dimethyl-l-propargylxanthine (DMPX, 10 microM) (a more specific adenosine A2 receptor antagonist), potentiated PAF activity on platelet aggregation in PRP samples containing adenosine. Also, patients receiving theophylline treatments showed significantly greater platelet aggregation induced by PAF in their PRP samples. PAF induced a rapid increase (80% in 15 sec) in intracellular Ca2+ mobilization, which was strongly inhibited by adenosine (IC50, 0.3 microM). Our studies suggest that agents that can increase plasma adenosine levels (e.g. inhibitors of adenosine uptake and adenosine metabolism) or methylxanthines may be useful in altering (inhibiting or enhancing, respectively) PAF actions on platelets and other tissues.

Adenosine↗
PubMed1993

The clinical usefulness of the platelet aggregation test for the diagnosis of heparin-induced thrombocytopenia.

The platelet aggregation test is widely used for the diagnosis of heparin-induced thrombocytopenia (HIT), a potentially serious complication of heparin therapy. We have evaluated its sensitivity and specificity in comparison with those of the 14C-serotonin release test. The sensitivity of the platelet aggregation test was found to vary with the heparin concentration and the donor of the platelets used in the test. The optimal heparin concentrations were between 0.1 and 1.0 U/ml. Using these heparin concentrations, the mean sensitivity varied from 39% (with the least reactive platelets) to 81% (with the most reactive platelets). In comparison, the sensitivity of the release test ranged from 65% to 94%. The specificities of the platelet aggregation test were 82%, 90% and 100% for the following control groups: (1) non-thrombocytopenic patients given heparin, (2) patients with thrombocytopenia due to other causes, and (3) normal controls not given heparin, respectively. The corresponding specificities for the release test was 94%, 90% and 100%. The specificities can be further increased to 100% for all controls with the adoption of a two-point system which defines a positive result as one in which platelet aggregation occurs with a low heparin concentration (0.5 U/ml) but not with 100 U heparin/ml. For optimal results, a two-point platelet aggregation test should be performed with heparin concentrations of 0.5 and 100 U/ml and using platelets of more reactive donors.

Autoimmune Diseases↗
PubMed1987

High sodium intake increases platelet aggregation in normal females.

Platelet activation and aggregation appear to play an important part in the development of vascular disease. We studied the effect of varying sodium intake on total plasma serotonin and in vitro aggregation of blood platelets. A total of 12 normal female volunteers were studied after 5 days on a 10 or 200 mmol/day sodium diet. Aggregation studies were performed by incubating stirred platelet-rich plasma (PRP) with adenosine diphosphate (ADP) at final concentrations of 1 and 4 mumol/l; we also studied the effect of pre-incubating PRP with ketanserin or saralasin (1 mumol/l and 1 nmol/l final concentration, respectively). Salt-loading produced a significant increase in platelet aggregation induced by both 1 and 4 mumol/l ADP, and also a significant fall in PRP in serotonin concentration; since there was also a significant drop in the yield of platelets in PRP during salt-loading, the difference in serotonin concentration was not significant when expressed as pmol serotonin/10(8) platelets. There was a significant negative correlation between log serotonin levels (nmol/l) and % aggregation induced by 4 mumol/l ADP. Ketanserin decreased aggregation (induced by 4 mumol/l ADP) in PRP obtained during high salt intake; saralasin had no effect on aggregation, but did cause a decrease in light transmission. These results indicate that in normal females: (1) in vitro platelet aggregation is increased with high sodium intake, and this effect was reduced by addition of ketanserin; (2) PRP platelet count and total plasma serotonin levels are both significantly altered by changes in sodium status; (3) aggregation (%) is inversely proportional to log serotonin concentration (nmol/l).

Adult↗
PubMed1991

Hydrogen peroxide as trigger of platelet aggregation.

In order to verify if H2O2 affects platelet function, platelet-rich plasma and human washed platelets were incubated with subthreshold concentrations (STC) of collagen or arachidonic acid or ADP and/or with 75-150 microM H2O2. While H2O2 alone did not affect platelet aggregation, it amplified platelet aggregation response in samples stimulated with STC of arachidonic acid and collagen but not in samples stimulated with STC of ADP. When platelets were preventively treated with aspirin, a cyclooxygenase inhibitor, the platelet activation by H2O2 was not observed. Thromboxane A2 (TxA2) was not produced by human washed platelets stimulated with STC of arachidonic acid, collagen or by H2O2 alone. On the contrary, when STC of agonists were tested on platelets supplemented with H2O2 an evident TxA2 production was seen. This effect was prevented by aspirin pretreatment or by the addition of catalase, an enzyme which destroys H2O2. This study suggests that H2O2 triggers the activation of platelets exposed to STC of collagen and arachidonic acid, via the cyclooxygenase pathway.

Adult↗
PubMed1994

Adenosine-mediated inhibition of platelet aggregation by acadesine. A novel antithrombotic mechanism in vitro and in vivo.

Inhibition of platelet aggregation by acadesine was evaluated both in vitro and ex vivo in human whole blood using impedance aggregometry, as well as in vivo in a canine model of platelet-dependent cyclic coronary flow reductions. In vitro, incubation of acadesine in whole blood inhibited ADP-induced platelet aggregation by 50% at 240 +/- 60 microM. Inhibition of platelet aggregation was time dependent and was prevented by the adenosine kinase inhibitor, 5'-deoxy 5-iodotubercidin, which blocked conversion of acadesine to its 5'-monophosphate, ZMP, and by adenosine deaminase. Acadesine elevated platelet cAMP in whole blood, which was also prevented by adenosine deaminase. In contrast, acadesine had no effect on ADP-induced platelet aggregation or platelet cAMP levels in platelet-rich plasma, but inhibition of aggregation was restored when isolated erythrocytes were incubated with acadesine before reconstitution with platelet-rich plasma. Acadesine (100 mg/kg i.v.) administered to human subjects also inhibited platelet aggregation ex vivo in whole blood. In the canine Folts model of platelet thrombosis, acadesine (0.5 mg/kg per min, i.v.) abolished coronary flow reductions, and this activity was prevented by pretreatment with the adenosine receptor antagonist, 8-sulphophenyltheophylline. These results demonstrate that acadesine exhibits antiplatelet activity in vitro, ex vivo, and in vivo through an adenosine-dependent mechanism. Moreover, the in vitro studies indicate that inhibition of platelet aggregation requires the presence of erythrocytes and metabolism of acadesine to acadesine monophosphate (ZMP).

Adenosine↗
PubMed1976

The variability of platelet-collagen interaction. Its influence on aspirin-induced inhibition of platelet aggregation.

A study of platelet aggregation induced by progressive concentrations of collagen was performed in 40 normal persons, equally grouped by sex, immediately before, and 90 min after, the ingestion of 0.500 g aspirin. Simultaneously, serum ASA-esterase activity and plasmatic salicylic acid levels were investigated in the pre- and post-ASA samples respectively. Wide individual variations in platelet responsiveness to collagen were found when the minimal amount of the aggregating agent necessary to provoke significant aggregation was located. The percentage of aggregation and the slope were the most sensible indicators of both the individual variances and the ASA-induced inhibition. Correlation was found in both groups between the minimal amounts of collagen required for initiating aggregation pre- and post-ASA. Also positive correlation was found between the minimal collagen concentration required to initiate aggregation pre-ASA and the aspirin-induced inhibition in the aggregation produced by a higher collagen concentration. Important individual and sexual differences were detected in the serum content of ASA-esterase activity. A negative significant correlation was demonstrated between the ASA-esterase activity and the differences in collagen concentrations necessary to start aggregation pre- and post-aspirin in the men group. Failure to consider individual variances in platelet reactivity may lead to false conclusions about the ASA affectiveness as an antithrombotic agent.

Adolescent↗
PubMed1996

Inhibitory effects of TA-993, a new 1,5-benzothiazepine derivative, on platelet aggregation.

TA-993, an l-cis 4',8-dimethyl derivative of the Ca2+ antagonist diltiazem, and some of its metabolites inhibited platelet aggregation induced by collagen, ADP, epinephrine, platelet activating factor, arachidonic acid, and U-46619 in human platelets in vitro. Among the metabolites, MB3 was the most potent (IC50, <1 micromol/L; several hundred times more potent than the parent compound). The d isomer of MB3 was >100 times less potent than the l isomer. Unlike acetylsalicylic acid (ASA), TA-993 inhibited both primary and secondary phases of ADP-induced platelet aggregation and also exhibited a disaggregating effect on human platelet aggregates. The inhibitory effect of TA-993 was enhanced when used in combination with ASA. In ex vivo studies involving rats, TA-993 (approximately 0.3 to 100 mg/kg PO) dose-dependently inhibited collagen-induced platelet aggregation (ED50, 3 mg/kg PO). In the whole-blood platelet aggregation system in rats, orally administered TA-993 was also inhibitory in single (3 to 30 mg/kg) or repeated daily (10 mg/kg per day for 10 days) dosage. Orally administered TA-993 dose-dependently inhibited ADP-induced platelet aggregation ex vivo in dogs (0.3 to 10 mg/kg), significantly protected mice against collagen + epinephrine-induced thromboembolic death (10 mg/kg), and inhibited thrombus formation in an arteriovenous shunt in rats (30 mg/kg). The Ca2+-antagonistic action of TA-993 was very weak in depolarized canine basilar arteries: the potency was approximately 1/10 that of diltiazem (d-cis) and d-TA-993. These results suggest that antiplatelet action is more characteristic of the l-cis than the d-cis 1,5-benzothiazepine structure and that TA-993 may become a clinically useful antiplatelet agent of this structure series.

Animals↗
PubMed1994

Platelet aggregation, coronary artery disease progression and future coronary events.

The platelet-aggregatory response, platelet-release factors and markers of thrombin generation in vivo were studied prospectively in 53 patients participating in a randomized clinical trial evaluating the influence of nicardipine on the progression of coronary atherosclerosis. Coronary lesions were measured quantitatively and progression was defined as a decrease in minimum diameter by > or = 0.4 mm. At repeat angiography 24 months after study entry, 20 of the 53 patients had progression of 28 coronary narrowings. Only thrombin-induced enhanced platelet aggregation differentiated patients with from those without coronary disease progression, with an estimated odds ratio of 2.49 (95% confidence interval 1.10 to 5.66). The aggregatory response to adenosine diphosphate, collagen, epinephrine and platelet-activating factor were not different in the 2 groups of patients, nor were measurements of platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-prostaglandin F1 alpha and fibrinopeptide A. During 46.8 months of follow-up after repeat angiography, coronary events occurred in 11 of the 20 with and 6 of the 33 without progression (difference 37%, p = 0.013, confidence interval 11 to 63%). Those with coronary disease progression and an enhanced thrombin-induced platelet aggregation had a worse prognosis than those with no disease progression and a low thrombin-induced platelet aggregation. Thus, patients with coronary disease progression and future coronary events have an enhanced thrombin-induced platelet aggregation. This platelet abnormality may be a marker of increased risk and may play a causative role in the development of coronary events.

6-Ketoprostaglandin F1 alpha↗
PubMed1976

Impairment of ADP-induced platelet aggregation by hashish components.

ADP-induced aggregation of washed human platelets is inhibited by the hashish components delta1-tetrahydrocannabinol (THC) and cannabidiol (CBD). The inhibition is counteracted by added ADP. When the cannabinoids are present at concentrations higher than 10(-5)M, the platelets aggregate non-reversibly, independently of an added inducer, apparently due to lysis and release of endogenous inducers. THC is clearly more potent than CBD in exhibiting the biphasic effect. Collagen- and thrombin-induced aggregation of washed platelets are hardly affected by the cannabinoids. THC and CBD also curtail ADP-induced reversible aggregation in platelet-rich plasma, while serotonin release and irreversible aggregation, caused by either ADP, collagen or thrombin, are not affected by the cannabinoids in platelet-rich plasma. The data point to associated sites for ADP and the cannabinoids on the platelet membrane.

Adenosine Diphosphate↗
PubMed2002

The effect of submaximal exercise on platelet aggregation during late follicular and midluteal phases in women.

INTRODUCTION: The key role of platelets in the pathogenesis of atherosclerosis prompted considerable interest on the effect of physical exercise on platelets. Due to probable menstrual cycle variations, only a limited number of investigations have studied the effect of exercise on platelets in women. The study was undertaken to determine the effect of acute submaximal exercise on platelet aggregation and thromboxane A(2) (TxA(2)) formation in females during their late follicular and midluteal phases. MATERIALS AND METHODS: Twelve healthy, sedentary, female volunteers performed 15 min of cycling exercise at a workload that increased their heart rate to 75% of maximal in two phases of the menstrual cycle. The maximal rate of ADP and collagen-induced platelet aggregation was evaluated on citrated whole blood using the impedance technique. Thrombin-induced thromboxane A(2) formation was evaluated by the measurement of thromboxane B(2) (TxB(2)) level by enzyme-linked immunoassay. RESULTS AND CONCLUSION: No significant difference was found between maximal rates of platelet aggregation measured in the different phases of menstrual cycle. Collagen-induced platelet aggregation and platelet count increased significantly after the exercise in both late follicular and midluteal phases (p<0.05). ADP-induced platelet aggregation did not change due to the exercise during the two phases of menstrual cycle. The thromboxane B(2) level measured in the midluteal phase was significantly higher than that measured in late follicular phase at rest. It was significantly increased after the exercise in late follicular phase while no significant difference was found between pre-exercise and postexercise levels in the midluteal phase. The differences in thromboxane A(2) formation were pointed out in the changes in platelet reactivity status. The inhibitory systems for platelets need further investigations. Our findings support the idea that menstrual variations do not have pronounced and acute effects on both platelet aggregation and response of platelets to acute exercise.

Adenosine Diphosphate↗
PubMed2004

Inhibition of platelet aggregation by aspirin progressively decreases in long-term treated patients.

OBJECTIVES: We sought to investigate, during a two-year follow-up period, the effects of aspirin on platelet aggregation. BACKGROUND: The platelets of patients given aspirin may be less sensitive to antiplatelet treatment, although the extent of such phenomenon over long-term follow-up is unclear. METHODS: Adenosine diphosphate (ADP) and collagen-induced platelet aggregation was periodically monitored before and after 2, 6, 12, and 24 months of treatment with aspirin (n = 150) or ticlopidine (n = 80) in patients matched for gender, age, and risk factors for atherothrombosis. RESULTS: Compared with baseline values, two months of aspirin treatment significantly inhibited platelet aggregation; thereafter, this inhibitory effect progressively decreased. At 24-month follow-up, collagen-induced platelet aggregation was significantly higher than that observed at two months (p < 0.05); a more pronounced difference was observed when collagen-induced lag phase was considered (p < 0.01). Restoration of platelet aggregation was less evident when ADP was used as an agonist. Conversely, the inhibition induced by ticlopidine was constant throughout follow-up with both agonists. CONCLUSIONS: The study demonstrates that a long-term treatment with aspirin is associated with a progressive reduction in platelet sensitivity to this drug.

Adenosine Diphosphate↗
PubMed1992

Recognition of platelet-associated fibrinogen by polyclonal antibodies: correlation with platelet aggregation.

Progressive decreases in platelet-bound fibrinogen accessibility to antibody and enzymes were recently reported to occur after adenosine diphosphate (ADP)-induced fibrinogen binding. Because previous studies also indicated that platelets that are activated but not aggregated by ADP in the presence of fibrinogen lose their ability to aggregate in a time-dependent manner despite negligible changes in fibrinogen binding, the present study examined the relationship between platelet aggregation and accessibility of platelet-bound fibrinogen to specific polyclonal antibody F(ab')2 fragments over a 60-minute time course. Although 125I-fibrinogen binding remained virtually unchanged, comparison of antifibrinogen antibody F(ab')2 binding and platelet aggregation 5 minutes and 60 minutes after platelet stimulation with ADP or thrombin showed decreases in F(ab')2 binding of 62% +/- 13% and 73% +/- 7% (mean +/- SD, n = 5), respectively, and decreases of 65% +/- 16% and 60% +/- 10% in platelet aggregation. In contrast, platelets stimulated with A23187 or chymotrypsin retained 87% +/- 16% and 76% +/- 12% of their ability to aggregate over the same time course, and lost only 39% +/- 14% and 36% +/- 12% of their ability to bind antifibrinogen antibody F(ab')2 fragments, respectively. Pretreatment of ADP-stimulated platelets with chymotrypsin largely prevented the progressive loss of platelet aggregability and the accompanying decreased recognition of bound fibrinogen by antifibrinogen F(ab')2 fragments. Preincubation of platelets with cytochalasin D (30 micrograms/mL) also inhibited the decrease in platelet aggregation after exposure of ADP-treated platelets to fibrinogen over a 60-minute time course. This was accompanied by only a 25% +/- 18% decrease in antifibrinogen antibody F(ab')2 binding. Present data support the hypothesis that qualitative changes in platelet-bound fibrinogen correlate with loss of the ability of platelets to aggregate, and implicate both the platelet cytoskeleton and chymotrypsin-sensitive surface membrane structures in modulating qualitative changes in bound fibrinogen on the platelet surface.

Adenosine Diphosphate↗
PubMed1995

Dehydroepiandrosterone inhibits human platelet aggregation in vitro and in vivo.

The hypothesis has been advanced that the adrenal steroids dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) exert antiatherogenic and cardioprotective actions. Platelet activation has also been implicated in atherogenesis. To determine if DHEA and DHEAS affect platelet activation, the effects of these steroids on platelet aggregation were assessed both in vitro and in vivo. When DHEAS was added to pooled platelet-rich plasma before the addition of the agonist arachidonate, either the rate of platelet aggregation was slowed or aggregation was completely inhibited. Inhibition of platelet aggregation by DHEA was both dose- and time-dependent. Inhibition of platelet aggregation by DHEA was accompanied by reduced platelet thromboxane B2 (TxB2) production. Inhibition of platelet aggregation by DHEA was also demonstrated in vivo. In a randomized, double-blind trial, 10 normal men received either DHEA 300 mg (n = 5) or placebo capsule (n = 5) orally three times daily for 14 days. In one man in the DHEA group arachidonate-stimulated platelet aggregation was inhibited completely during DHEA administration, whereas in three other men in the DHEA group the rate of platelet aggregation was prolonged, and the sensitivity and responsiveness to agonist were reduced. None of the men in the placebo group manifested any change in platelet activity. These findings suggest that DHEA retards platelet aggregation in humans. Inhibition of platelet activity by DHEA may contribute to the putative antiatherogenic and cardioprotective effects of DHEA.

Dehydroepiandrosterone↗
PubMed1979

Chromatographic fractionation and characterization of the active platelet aggregation inhibitory factor from bromelain.

Isolation and characterization of the platelet aggregation inhibitory factor of bromelain have been presented in this study. Commercial bromelain consists of 3 major components as demonstrated by discontinuous sodium chloride gradient chromatography through carbixymethyl-sephadex column. Fraction I constituted approximately 19% of the total fraction. This fraction had no proteolytic activity or platelet aggregation inhibiting activity, but showed peroxidatic activity. Fraction II and III, which constituted the remainder of the fraction eluted with 135 mM and 800 mM NaCl concentrations, respectively, showed both proteolytic and inhibition of platelet aggregation, but no peroxidatic activity. Immunoelectrophoresis and polyacrylamide electrophoresis showed fraction I with beta-mobility while fraction II and III demonstrated gamma-mobility. It is suggested that the proteolytic activity is associated with the inhibition of platelet aggregation, since oxidation of fractions II and III with sodium tetrathionate abolished both activities. The mechanism of inhibition of platelet aggregation by bromelain is presently unknown but may involve its influence on the prostaglandin synthetic pathway of platelets.

Bromelains↗
PubMed2005

Acute microvascular platelet aggregation after subarachnoid hemorrhage.

OBJECT: The mechanisms underlying acute cerebral ischemia after subarachnoid hemorrhage (SAH) are not well established. Platelets aggregate within major cerebral vessels hours after SAH, but this has not been studied in the microvasculature. Platelet aggregates within the microvasculature could mechanically obstruct the lumen and initiate events that injure vessel structure. In the present study the authors examined the hypothesis that platelets aggregate within the cerebral microvasculature acutely after SAH. METHODS: Subarachnoid hemorrhage was induced in the rat by using the endovascular perforation model. The animals were killed between 10 minutes and 48 hours after SAH. Immunostaining for the platelet surface receptor glycoprotein (GP)IIb/IIIa, which mediates platelet aggregation, was used to detect platelet aggregation. Sham-operated animals were used as controls. The GPIIb/IIIa immunoreactive platelet aggregates were abundant in the microvasculature of the basal and frontal cortex, striatum, and hippocampus 10 minutes after SAH. These aggregates decreased in number from 1 to 6 hours post-SAH and then increased to a peak at 24 hours. No immunoreactive aggregates were observed 48 hours after SAH. CONCLUSIONS: The data indicate that widespread platelet aggregation occurs very rapidly in response to SAH followed by a decrease within 6 hours and a subsequent increase 24 hours after SAH. Microvascular platelet aggregates may contribute to decreased cerebral blood flow and ischemic injury after SAH via a number of mechanisms.

Acute Disease↗
PubMed2003

Mechanisms involved in adenosine triphosphate--induced platelet aggregation in whole blood.

OBJECTIVE: Effects on platelet aggregation of adenosine triphosphate (ATP) released from damaged cells and from platelets undergoing exocytosis have not been clearly established. In this study we report on the effects of ATP on platelet aggregation in whole blood. METHODS AND RESULTS: Aggregation, measured using a platelet-counting technique, occurred in response to ATP and was maximal at 10 to 100 micromol/L. It was abolished by MRS2179, AR-C69931, and creatine phosphate/creatine phosphokinase, implying that conversion to adenosine diphosphate (ADP) is required. ATP did not induce aggregation in platelet-rich plasma, but aggregation did occur when apyrase or hexokinase was added. Aggregation also occurred after addition of leukocytes to platelet-rich plasma (as a source of ecto-ATPase), and this was potentiated on removal of adenosine by adenosine deaminase, indicating that adenosine production modulates the response. Dipyridamole, which inhibits adenosine uptake into erythrocytes, inhibited aggregation induced by ATP in whole blood, and adenosine deaminase reversed this. DN9693 and forskolin synergized with dipyridamole to inhibit ATP-induced aggregation. CONCLUSIONS: ATP induces aggregation in whole blood via conversion of ATP to ADP by ecto-ATPases on leukocytes. This is inhibited by agents that prevent adenosine removal. Reduced aggregation at high concentrations of ATP (>100 micromol/L) may be a consequence of inhibition by ATP of ADP action at ADP receptors.

Adenosine Deaminase↗
PubMed1982

Relationship between platelet aggregation, thromboxane synthesis and albumin concentration in nephrotic syndrome.

Increased platelet aggregability on stimulation with sodium arachidonate (NaAA), collagen and ADP was found in a group of 14 patients with nephrotic syndrome when compared with age and sex matched controls. Five of the group also exhibited spontaneous platelet aggregation (SPA), associated with synthesis of thromboxane B2 (TxB2), and which appeared to correlate with a markedly increased serum triglyceride concentration. Thromboxane B2 generation in response to NaAA was increased and reflected both the low serum albumin concentration and the platelet aggregation response to this agent. Addition of albumin in vitro decreased the amount of TxB2 generated for a given dose of NaAA and increased NaAA and collagen-induced platelet aggregation thresholds. However, albumin had no significant effect on collagen-induced TxB2 production. The results suggest that the hypoalbuminaemia and associated reduced binding of arachidonic acid and increased synthesis of TxA2 account in part for the increased platelet aggregability seen in the nephrotic syndrome but that other mechanisms are also involved.

Adenosine Diphosphate↗
PubMed1999

Effect of systemic alpha-2 adrenergic blockade on the morning increase in platelet aggregation in normal subjects.

To assess whether activation of platelets by catecholamines contributes to the increase in platelet aggregation associated with either the assumption of upright posture or exercise, we studied the effect of oral yohimbine on these phenomena. Whole blood platelet aggregation and plasma catecholamine levels were measured before and after standing and at peak exercise in untreated normal subjects and after oral yohimbine. Neurochemical indexes indicated systemic alpha2-receptor blockade by yohimbine. Yohimbine reduced the orthostatic increase in platelet aggregation response by 63+/-11%, but exercise-induced increase in aggregation was unaffected. Thus, alpha2-adrenergic blockade attenuates the orthostatic increase in platelet aggregation. Agents designed to inhibit the morning surge in catecholamine levels or block platelet alpha2 adrenoceptors may reduce the risk of thrombotic vascular events in atherosclerosis.

Adrenergic alpha-2 Receptor Antagonists↗