Platelet-stimulated thrombin and PDGF are normalized by insulin and Ca2+ channel blockers

Department of Medicine, Mount Sinai School of Medicine, New York 10029; and Spinal Cord Damage Research Center, Veterans Affairs Medical Center, Bronx, New York 10468 Coronary artery disease is accelerated in chronic spinal cord injury (SCI). Because prostacyclin (PGI 2 ) may retard atherogenesis th...

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Bibliographic Details
Published in:American journal of physiology: endocrinology and metabolism 1999-05, Vol.276 (5), p.E856
Main Author: Kahn, Nighat N
Format: Article
Language:English
Online Access:Get full text
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Summary:Department of Medicine, Mount Sinai School of Medicine, New York 10029; and Spinal Cord Damage Research Center, Veterans Affairs Medical Center, Bronx, New York 10468 Coronary artery disease is accelerated in chronic spinal cord injury (SCI). Because prostacyclin (PGI 2 ) may retard atherogenesis through its inhibitory effects on platelet function, the role of PGI 2 on SCI platelets was determined. The SCI platelets were neither hypersensitive to aggregating agonists nor resistant to the inhibitory effect of PGI 2 , but PGI 2 failed to inhibit platelet-stimulated thrombin generation and the release of platelet-derived growth factor (PDGF) in SCI. Because thrombin and PDGF are atherogenic mitogens, the generation of these mitogens was investigated. Both the release of PDGF and thrombin generation in SCI platelets were higher when compared with control ( n  = 12). Treatment of non-SCI platelets with 100 nM PGE 1 (a stable probe of PGI 2 ) inhibited the release of the mitogens by 90% ( P  
ISSN:0193-1849
1522-1555
DOI:10.1152/ajpendo.1999.276.5.e856