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|Title:||Increase membrane vesiculation in essential hypertension|
Chotiros D. Plabplueng
|Keywords:||Biochemistry, Genetics and Molecular Biology;Medicine|
|Citation:||Laboratory Medicine. Vol.43, No.1 (2012), 6-9|
|Abstract:||Background: A hypertensive condition is known to be an important risk factor for arterial disease and thrombotic events. The detailed understanding of the pathophysiology in thrombotic events is crucial for the development of both preventive measures and the treatment during the early stage. Microparticles are submicron cell membrane vesicle shed from the cell surface in response to cell injury or apoptosis, and they are an essential element in the process leading to the pathogenesis of thrombosis and hemostasis dysfunction in patients. Activation of blood cells can result in the formation of microparticles, which carry a negatively charged, phosphatidylserine (PS), with a diameter of < 1.0 micron. The biological and clinical functions of microparticles have been highlighted in coronary artery disease and heart failure. Objective: To elucidate the functional role of microparticles in essential hypertension. Methods: We quantitated the total number of circulating PS+ microparticles and studied the role of PS+ microparticles to see whether they can shorten the plasma recalcification time in patients with essential hypertension. Results: The PS+ microparticles were detectable at a low level in healthy blood and significantly increased in the patients with essential hypertension. With regard to PS+ microparticles affecting prothrombotic state in hypertension, we enriched microparticles and determined their procoagulant activity with a plasma recalcification time. The clotting time was significantly reduced after the addition of enriched microparticles to plasma poor microparticles (PPMP). A significant negative correlation was detected between numbers of enriched-PS+ microparticles and plasma-clotting time (r=-0.43, P=0.01). Conclusion: Taken together, high levels of PS+ microparticles are present in the circulating blood of essential hypertension and may contribute to the generation and perpetuation of a thrombotic state.|
|Appears in Collections:||Scopus 2011-2015|
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