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  • 1
    ISSN: 1423-0127
    Keywords: Plasmin ; Calcium influx ; Cytosolic phospholipase A2 ; Endothelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Treatment of cultured bovine carotid artery endothelial cells with 0.1 µM human plasmin has been reported to induce a receptor-mediated short burst of arachidonate release, which is a pertussis toxin-sensitive and extracellular calcium-dependent reaction. Plasmin-induced calcium influx in cells was significantly inhibited by pretreatment with pertussis toxin, indicating that the former was coupled with a pertussis toxin-sensitive guanosine 5′-triphosphate (GTP)-binding protein. Plasmin significantly induced the formation of lysophosphatidylcholine but not lysophosphatidylethanolamine. A cellular phospholipase A2 with an arachidonyl specificity at the sn-2 position of phosphatidylcholine, which required submicromolar calcium, was identified as a cytosolic phospholipase A2 by immunoblot analysis. By a cell-free enzyme activity assay and immunoblot analysis, plasmin was found to induce a translocation of the cytosolic phospholipase A2 from the cytosol to the membrane. Taken together, the results suggest that plasmin bound to its putative receptor and activated a GTP-binding protein coupled to calcium influx channel, followed by translocation and activation of cytosolic phospholipase A2 in endothelial cells.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1423-0127
    Keywords: Acetylcholine ; Sodium nitroprusside ; Receptor-mediated processes ; Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract This study investigated the effects of exercise training on the regional release of endothelium-derived nitric oxide (EDNO) in spontaneously hypertensive rats (SHR). Male SHR and Wistar-Kyoto rats were divided into control and training groups, respectively. The training groups received moderate exercise by running on a drum exerciser for 60 min/day, 5 days/week for 10 weeks. At the end of experiments, thoracic aortae and common carotid arteries were excised. Acetylcholine (ACh)-induced relaxing responses due to EDNO release were evaluated in the presence of indomethacin. Vascular relaxing responses to A23187 or to sodium nitroprusside (SNP) were also studied. Our results indicated that after training, (1) the vascular sensitivity of thoracic aortae to ACh-induced relaxation was elevated when indomethacin was present; this effect was absent in the common carotid artery and it was abolished by adding Nω-nitro-L-arginine, and (2) no significant changes in SNP- or A23187-induced vascular relaxing responses, both being nonreceptor-mediated processes, were observed. We can conclude that for both hypertensive and normotensive rats, exercise training may increase receptor-mediated agonist-stimulated EDNO release in the thoracic aorta, but not in the common carotid artery.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1423-0127
    Keywords: Receptor assay ; M3 receptor ; α2-Adrenergic receptor ; Endothelium-derived nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The effects of acute exercise on receptor-mediated endothelium-dependent vasodilation and its possible mechanisms were investigated in the presence of indomethacin. Male Wistar rats (16–20 weeks old) were divided into control and exercise groups. The exercise group ran on a drum exerciser until exhaustion, followed by immediate decapitation. Acetylcholine (ACh)- or clonidine (CLO)-induced vasodilating responses in thoracic aortae of the control and exercise groups were compared. Receptor-binding assays were performed to determine whether there were any upregulations of endothelial receptors after acute exercise. Our results indicated that acute exercise induced the following effects: (1) the dose-response curves of ACh and CLO shifted to the left; (2) the high-affinity M3 binding sites increased in number but not in affinity; (3) the α2 binding sites decreased in number but increased in affinity. We conclude that acute exercise enhances receptor-mediated vasodilation responses, at least in part, by regulating either endothelial receptor number or receptor affinity.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 2 (1982), S. 445-455 
    ISSN: 0886-1544
    Keywords: clot structure ; platelet contractility ; protein networks ; rheological techniques ; viscoelasticity ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: When citrated plasma is recalcified, it forms a viscoelastic gel-a clot. The relationship between platelet contractility and clot rigidity was studied by using a rheological technique which simultaneously measured both the dynamic rigidity modulus and the contractile force during gel formation with platelet rich plasma (PRP). Protein network formation in a clot was accompanied by a contractile force throughout the clotting process. PRP demonstrated a maximum elastic modulus of 6,000 dynes/cm2 and a maximum contractile force/area of 1,500 dynes/cm2. The values of these parameters for a platelet-free clot (PFP) were 700 dynes/cm2 and less than 100 dynes/cm2 respectively. Sonicated control PRP and PRP from a Glanzmann thrombasthenia patient both clotted in a manner similar to PFP. Metabolic inhibitors, 2-deoxy-D-glucose and KCN (5 mM each), retarded the clotting curves of PRP. Cytochalasin B and E suppressed both structural rigidity and force generation in a concentration-dependent manner similar to their inhibitory effect on actin polymerization in platelets. Colchicine (2.5 mM) or vinblastine (0.11 mM) did not affect these clotting curves. Thrombi-activated, fixed platelets did not generate any force, nor did they significantly increase clot rigidity. Streptokinase induced a concurrent decrease of both rigidity and force in PRP clots. The elastic modulus of a PFP clot could be increased to 2,500 dynes/cm2 by externally straining the network with an axial force/area of 1,500 dynes/cm2. Our results indicate that clot structure formation in PRP is strongly coupled to the contractile force generated by the platelet microfilament system and that this force modulates clot rigidity.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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