Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:001400 (PRP)
 1,320 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparative study of ADP-induced aggregation was made in adult rabbits' intact and refractory platelets and in 7-day rabbits' platelets in vitro. Platelets of the young animals resembled refractory those of adults. The effect of ADP on platelets in vivo did not depend on the age of animals. Changes in platelet population composition of adult and 7-day rabbits during standard isolation procedure were compared. The platelets in PRP of young rabbits were damaged to a greater extent than those of adult animals. It is suggested that the refractory state of young animal platelets in PRP as obtained with the standard technique, could be attributed to their decreased resistance against mechanical forces.
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PMID:[A comparative study of the functional characteristics of thrombocytes at different stages of individual development]. 121 91

In the PRP of anaphylactic rats, ADP, collagen and thrombin induced platelet aggregation was considerably reduced. Reduced aggregability could be transferred to normal platelets by suspending them in the PPP of anaphylactic animals and the impaired aggregation of platelets from animals undergoing anaphylaxis could be restored by exchanging their plasma for that of normal controls. Ellagic acid, a known activator of factor XII, produced similar alterations as obtained in anaphylactic shcok. It is suggested that the inhibition of platelet aggregation is due to the anaphylactic activation of factor XII and this mechanism may be of importance in rat anaphylaxis.
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PMID:Reduced aggregability of platelets in rat anaphylaxis. 126 97

Rhynchophylline (Rhy) inhibited rabbit platelet aggregation induced by arachidonic acid (AA), collagen, and ADP. The values of IC50 were 0.72, 0.74, and 0.67 mmol.L-1, respectively. Rhy reduced the thromboxane B2 (TXB2) generation in PRP induced by collagen but failed to reduce that induced by AA. Rhy suppressed malondialdehyde (MDA) formation in platelet suspension stimulated by thrombin, inhibited the platelet factor 4 (PF4) release. It did not alter intraplatelet cAMP concentration. Rhy 10-20 mg.kg-1 iv showed a significant inhibition of venous thrombosis and cerebral thrombosis in rats.
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PMID:Inhibitory effect of rhynchophylline on platelet aggregation and thrombosis. 131 85

Treatment of perfused rat hearts with 0.5 mM iodoacetamide (IAAm) for 15 min at different workloads resulting in a nearly complete inhibition of creatine kinase (CK, 99%) was followed by a rapid decline of the phosphocreatine (PCr) level (30%) and a 2-fold increase of the P(i) level which then stabilized. Conversely, the ATP content started to drop monotonously at the beginning of the IAAm washout and reached 30% 90 min after the IAAm removal under medium load. Under low workload the ATP decay occurred at later periods. Neither the ADP-stimulated mitochondrial respiration in skinned fibers, nor the Ca(2+)-stimulated ATPase activity of myofibrils was affected by IAAm treatment. The sensitivity of the resting tension of skinned fibers to Ca2+ tended to a slight increase. The cardiac work index (PRP-pressure-rate product) decreased by 25%, while the end diastolic pressure (EDP) rose by 15 mm Hg when IAAm acted under medium load. In contrast, under low work these parameters were practically stable. The hearts poisoned with IAAm performed a two times lower maximal work and had reduced (by 35%) oxygen consumption rates. The efficiency of energy utilization for mechanical work decreased by 40%. The changes in PRP and EDP correlated with the cytosolic [ATP]/[ADP] ratio in such a way that the decrease in the latter was associated with a decrease in PRP and the elevation of EDP. These data suggest that the creatine kinase system is necessary for the effective translation of a high [ATP]/[ADP] ratio from the intermembrane space of mitochondria to the cytoplasm, myofibrils and ionic pumps. This provides a high level of mechanical work and good relaxation of the left ventricle and protects cytosolic adenine nucleotides from the breakdown.
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PMID:[Metabolic and functional consequences of complete inhibition of creatine kinase by iodoacetamide in the perfused heart]. 138 56

Two heavy metals, lead and cadmium, are frequently found as pollutants in many systems. Their effect upon platelet aggregation was investigated, both in human and rat platelet rich plasma and washed platelets. ADP-induced aggregation of human platelets was inhibited by 50%, using concentrations of free lead between 2-4 mM and free cadmium between 0.05 and 0.2 mM. Rat platelets were about ten times more sensitive to the effect of lead than human PRP. 50% inhibition of epinephrine-induced aggregation was attained at lower concentrations of metal, than the concentrations needed for ADP-induced aggregation. The effect was more apparent upon the first phase, which was lengthened, both with PRP and washed platelets. The aggregation of human and rat washed platelets by calcium was inhibited by concentrations of the metals within micromolar ranges. When A 23187 was used as the aggregating agent, the inhibition by the metals was only partial. Cysteine, at approximately tenfold concentrations, reversed the effect of the metals. Cadmium appeared more effective than lead as an inhibitor of platelet aggregation in all systems. Since only high levels of metal inhibit aggregation, more sensitive organs or systems would show alterations, due to these metals at an earlier stage and at lower concentrations.
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PMID:[Effect of lead and cadmium on platelet aggregation]. 141 49

The tetrapeptide H-Arg-Gly-Asp-Ser-OH (1) (RGDS), representing a recognition sequence of fibrinogen for its platelet receptor GP IIb-IIIa (integrin alpha IIb beta 3), served as lead compound for the development of highly potent and selective fibrinogen receptor antagonists. Replacement of the N-terminal arginine by p-amidinophenylalanine or the Gly moiety by m-aminobenzoic acid led to compounds which are superior to the lead peptide with regard to activity and selectivity for GP IIb-IIIa vs the closely related vitronectin receptor alpha v beta 3. By random screening [(p-amidinobenzenesulfonamido)ethyl]-p-phenoxyacetic acid derivatives have been identified as fibrinogen receptor antagonists. Further structure-activity relationship studies culminated in the preparation of N-[N-[N-(p-amidinobenzoyl)-beta-alanyl]-L-alpha-aspartyl]-3-phenyl-L- alanine (29h, Ro 43-5054) and [[1-[N-(p-amidinobenzoyl)-L-tyrosyl]-4-piperidinyl]oxy]acetic acid (37f, Ro 44-9883), which exhibit very high activity as platelet aggregation inhibitors (IC50s 0.06 and 0.03 microM, respectively, human PRP/ADP) as well as marked selectivity for GP IIb-IIIa vs alpha v beta 3. Since the activity of 37f in dogs declines according to a two-compartment model with an initial phase having a t1/2 of 8 min and a second phase with a t1/2 of 110 min, this compound is a suitable candidate for the development as iv platelet inhibitor.
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PMID:Low molecular weight, non-peptide fibrinogen receptor antagonists. 144 40

We have investigated the effect of varying sodium intake on the renin-angiotensin system, ADP-induced platelet aggregation in vitro, and blood 5-HT concentrations in 9 male volunteers. Systolic blood pressure was slightly reduced during a low sodium diet, whereas the diastolic pressure remained unchanged. Plasma renin activity and aldosterone concentration both fell significantly when sodium intake was increased; plasma angiotensin II concentration also fell, but not significantly. There was a significant fall in haematocrit after an increased sodium intake, but there was no change in the whole-blood platelet count after correcting for this. There were no significant changes in either total (i.e. PRP) or platelet 5-HT concentrations. The extent of platelet aggregation induced by 5 and 20 mumol.l-1 of ADP increased significantly when dietary sodium intake was increased. When compared with low or normal sodium intakes, lower concentrations of ADP were required to produce 50% of maximum aggregation after a high sodium intake. The 5-HT2 receptor antagonist ketanserin (1 mumol.l-1 in vitro) reduced the extent of aggregation induced by 5 mumol.l-1 ADP after the volunteers had taken a high sodium diet, whereas the angiotensin II receptor antagonist saralasin (1 nmol.l-1) increased the rate of aggregation after the low sodium diet. Thus, during a high sodium intake, human platelets become more sensitive to the aggregating agent ADP. It is possible that this effect is mediated via platelet 5-HT2 receptors, since ketanserin abolished the increase in salt-induced aggregation seen with 5 mumol.l-1 ADP.
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PMID:The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men. 149 45

The effect of severe reduction of cytosolic adenine nucleotide (AdN) pool and [ATP]/[ADP] ratio (by 2-deoxyglucose treatment) on functional and metabolic responses of isovolumic rat heart to increased energy demand induced by coronary flow (CF) rise and isoproterenol (Iso) addition has been investigated. AdN-depleted hearts had reduced phosphocreatine (PCr, by 80%), ATP (by 75%), [ATP]/[ADP] (24 times) and pressure-rate product (PRP, by 60%). An elevation of CF was followed by the increase in PRP in control and AdN-depleted hearts by 40-45% with unchanged metabolic parameters. At increased CF, Iso caused a further rise in PRP in both groups due to elevation of heart rate; however maximal levels of PRP in the AdN-depleted group still remained lower than that of control (by 40%). Only in control experiments was Iso addition accompanied by an increase in the difference between left-ventricular end- and minimal diastolic pressure, cytosolic [Pi] and [ADP], and some decrease in PCr and [ATP]/[ADP]. These data imply that severely reduced cytosolic [ATP]/[ADP] does not prevent acceleration of Ca2+ turnover by Iso in cardiomyocytes, it but restricts maximal force development affecting the myofibrils.
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PMID:Adrenergic stimulation of rat hearts with severely reduced cytosolic adenine nucleotide pool and [ATP]/[ADP]ratio. 159 Jul 36

In this highly controlled trial, 26 normolipidemic men (average age 28 years, range 18 to 60) were fed a baseline diet high in milk fat (MF) (fat 36% of energy, saturates 19%, monounsaturates 11%, polyunsaturates 4%), followed by a diet high in sunflower oil (SO) (fat 38% of energy, saturates 13%, monounsaturates 10%, polyunsaturates 13%) and another diet high in low erucic-acid rapeseed oil (RO) (fat 38% of energy, saturates 12%, monounsaturates 16%, polyunsaturates 8%). All diets were mixed natural diets with the same cholesterol contents. The baseline milk fat diet was given for 14 days and the oil diets for 24 days in a blind cross-over design. The platelet in vitro aggregation (slope %/min) induced by 1, 2 and 3 microM ADP and collagen (25 micrograms/ml PRP) was highly significantly (p less than 0.001) increased after both oil diets when compared with the results from the milk fat diet. The aggregation pattern determined by threshold collagen concentration confirmed increased collagen sensitivity of the platelets after the rapeseed oil diet (p less than 0.001). The enhancement of platelet aggregation was associated with increased in vitro platelet thromboxane production after the oil diets vs. the milk fat diet (p less than 0.05 after the sunflower oil diet and p less than 0.001 after the rapeseed oil diet).
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PMID:Rapeseed oil and sunflower oil diets enhance platelet in vitro aggregation and thromboxane production in healthy men when compared with milk fat or habitual diets. 164 26

Dipyridamole is widely used as a platelet function inhibitory drug. Its effect on platelet aggregation was investigated in a newly developed system, in which platelet aggregation was carried out in the presence of a human endothelial cell monolayer (EC). After iv. injection of 20 mg Dipyridamole platelet aggregation (inducer ADP 5 microM, Collagen 5 micrograms) was totally inhibited. The EC dependent antiaggregatory effect of Dipyridamol could be abolished if EC's were pretreated with 1 mmol ASA for 30 min. Our results, carried out in PRP demonstrate that Dipyridamole inhibits platelet aggregation even in the absence of red blood cells which were supposed to enhance the antiplatelet effect by their reduced adenosine uptake. Anenhanced PGI2 production in the EC's may explain the aggregation inhibiting effect of Dipyridamole in this test system.
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PMID:[Inhibition of induced thrombocyte aggregation in the presence of endothelial cells by dipyridamole]. 177 24


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