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Hypertension Research
Vol. 25 (2002) No. 3 May P 419-425

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http://doi.org/10.1291/hypres.25.419

Experimental studies

The cellular mechanisms by which hypertension enhances atherosclerosis are still not known in detail. Recently, evidence has been obtained that oxidative stress plays a role in the pathogenesis of pressure-induced atherosclerosis. We examined the effects of pressure on oxidative stress in cultured human coronary smooth muscle cells (SMCs). Application of increased pressure (+100 mmHg) with He gas for 48 h increased oxidative stress of measured by flow cytometry by 71% and F2-isopretane by 77%. Increased pressure also increased the activities of phospholipase D (PLD), and particulate protein kinase C (PKC). The PLD inhibitor suramin 100 μmol⁄l, 1-butanol 40 mmol⁄l, and the PKC inhibitors chelerythrine 1 μmol⁄l and calphostin C 100 nmol⁄l and completely blocked the increase in oxidative stress induced by pressure. Carvedilol 1 μmol⁄l but not propranolol 1 μmol⁄l blocked pressure-induced increases in oxidative stress in cultured SMCs. These findings suggest that pressure increases oxidative stress and that carvedilol significantly inhibits pressure-induced increase in oxidative stress in cultured human coronary smooth muscle cells. (Hypertens Res 2002; 25: 419-425)

Copyright © 2002 by the Japanese Society of Hypertension

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