Disease relevance of adenosine pyrophosphate

• At 0.1 and at 0.2 mg/kg body weight, 74% and 92% of the glycoprotein IIb/IIIa receptors were blocked, respectively; adenosine-diphosphate-induced platelet aggregation was inhibited by 84% and 100% at these same doses [1].
• In thrombocytovascular hemostasis, thrombocytopathy demonstrated increased adenosine-5-diphosphate aggregation and suppression of the internal route of fibrinolysis and endotheliosis [2].
• Fibrinogen was significantly correlated with collagen- and adenosine-diphosphate-induced platelet aggregation and with platelet adherence, spreading, and thrombus formation on subendothelium [3].
• Toxin preparations from Aeromonas spp. that completely inhibited adenosine-5'-diphosphate-induced platelet aggregation, an effect related to elevation of intracellular cAMP, were, with one exception, cross reactive with CT in ELISA [4].
• Adenosine-5'-diphosphate (ADP)-induced platelet aggregation failed to show significant differences between controls and subjects with a varying severity of retinopathy by either LS or LT, which indicates that SPA is more sensitive than agonist-induced platelet aggregation in relation to diabetic complications [5].

High impact information on adenosine pyrophosphate

• First, pretreatment of a human microvascular endothelial cell line (HMEC-1) with methotrexate increases extracellular adenosine after exposure of the pretreated cells to activated neutrophils; the ecto-5'-nucleotidase inhibitor alpha, beta-methylene adenosine-5'-diphosphate (APCP) abrogates completely the increase in extracellular adenosine [6].
• Arachidonic acid induced platelet aggregation was completely inhibited whereas that elicited by adenosine-5'-diphosphate was unaffected [7].
• In this study, we show that platelets activated with either adenosine-5'-diphosphate or epinephrine induce IL-8 secretion by EC [8].
• Our data indicate that platelets activated in platelet-rich plasma (PRP) by adenosine-5'-diphosphate (ADP) or thrombin bind plasminogen to their surface [9].
• Platelet GDH from these patients and controls was regularly inactivated by 2 mM guanosine-5'-triphosphate (GTP) and simulated one- to twofold by 2 mM adenosine-5'-diphosphate (ADP) [10].

Biological context of adenosine pyrophosphate

• A membrane-bound enzyme in rabbit aorta capable of inhibiting adenosine-diphosphate-induced platelet aggregation [11].
• Despite universal depletion of intraplatelet amines and alpha-granule contents only four out of 14 early allograft recipients had an abnormal bleeding time, and platelet aggregation thresholds with adenosine-5'-diphosphate and collagen were not different from controls [12].
• In thrombocyte vascular hemostasis, thrombocytopathy was observed with increased adenosine-5-diphosphate aggregation and the inhibition of the inner mechanism with fibrinolysis and endotheliosis [13].
• Adenosine-5'-triphosphate was synthesized by the phosphorylation of adenosine-5'-diphosphate in aqueous solution containing cyanate as a condensing reagent and insoluble calcium phosphate produced from phosphate and calcium chloride [14].
• Studies of patients with defective adenosine-5'-diphosphate mediated aggregation, as well as P2Y(12)-null mice, have revealed the importance of this receptor in mediating platelet activation and aggregation [15].

Anatomical context of adenosine pyrophosphate

• Adenosine-triphosphate (ATP), adenosine-diphosphate (ADP), glucose, and lactate were measured in the stroma and endothelium of 30 human corneas [16].
• Before the exercise, after its termination, and after 30 minutes of restitution the concentrations of adenosine-5' triphosphate, adenosine-5' diphosphate, adenosine-5' monophosphate, 2,3-diphosphoglycerate, nicotinamide-adenine dinucleotide and nicotinamide-adenine dinucleotide phosphate were assayed in erythrocytes [17].

Associations of adenosine pyrophosphate with other chemical compounds

• Primary platelet aggregation, induced by adenosine-diphosphate, is inhibited by piretanide, in vivo [18].
• We evaluated the effect of dipyridamole ex vivo and in vitro on platelet aggregation induced by collagen and adenosine-5'-diphosphate (ADP) in human whole blood with an impedance aggregometer [19].
• Decreasing the levels of endogenous adenosine by increasing the concentration of adenosine deaminase and adding the 5'-nucleotidase inhibitor alpha-beta-methylene adenosine-5'-diphosphate gave an increase in [3H]8-cyclopentyl-1,3-dipropylxanthine binding and diminished the response to GTP [20].
• The effects of a potent P2Y1 receptor antagonist, N6-methyl-2'-deoxyadenosine-3',5'-bisphosphate (MRS2179) on adenosine-5'-diphosphate (ADP)-induced platelet aggregation in vitro, ex vivo and on the bleeding time in vivo were determined [21].
• Structural data of an active phosphoglycolipid are also provided. trans-Resveratrol demonstrated also a dose-dependent inhibition of PAF-induced platelet aggregation along with the already reported inhibitory activity against thrombin and adenosine-5'-diphosphate [22].

Gene context of adenosine pyrophosphate

• In sections treated with adenosine deaminase and alpha-beta-methylene adenosine-5'-diphosphate, GTP steadily decreased [3H]N6-cyclohexyladenosine binding in all regions [20].
• After stimulation with adenosine-5-diphosphate (ADP) or the thrombin receptor agonist protein TRAP-6, platelet-leukocyte adhesion and surface expression of CD62P on platelets were evaluated by flow cytometry [23].
• Platelet-rich plasma (PRP) was incubated with CT 0-8 min after addition of the aggregation agonist (10 microM adenosine-5'-diphosphate, ADP, or 5 microg/ml collagen) and the aggregation was monitored [24].
• Venous blood samples (20 ml) were obtained before, immediately after exercise and at the end of recovery and were analysed for platelet indices, platelet aggregation using collagen and various final concentrations of adenosine-5'-diphosphate (ADP), and beta thromboglobulin (B-TG) [25].
• When platelets become activated by various soluble agonists or by adhesion to subendothelium under high shear, they release adenosine-5'-diphosphate that acts in a positive feedback mechanism on two different G-protein coupled receptors (P2Y(12), P2Y(1)) on platelets [15].

Analytical, diagnostic and therapeutic context of adenosine pyrophosphate

• Adenosine-diphosphate (ADP)-induced aggregation was measured and platelet adhesion to fibrinogen and collagen was measured in a perfusion chamber at shear rates of 300/sec and 1600/sec [26].
• Transmission and scanning electron microscopy indicate that rabbit platelets incubated in protein-poor medium retain their reactivity to shape change-inducing agents such as 5-hydroxytryptamine, adenosine-5'-diphosphate and chlorpromazine [27].
• In rats, the intravenous injection of 1 mg/kg A.D.P. (adenosine-5'-diphosphate) results in transient thrombocytopenia, bradycardia and arrhythmias [28].
• In an affected bull calf, initially evaluated because of excessive bleeding from a vaccination site, the platelet aggregation response to the agonist, adenosine-diphosphate (ADP) was essentially absent and the aggregation response to platelet activating factor (PAF16) was reduced by at least 70% [29].

References