Abstract
The carbon centered radicals generated by preincubation of cumene hydroperoxide with rat cardiac membranes dose dependently reduced the Bmax of [3H]nitrendipine binding, while KD was unchanged. The reduction induced by cumene hydroperoxide was prevented by 2,6-di-t-butlyl-4-methyl-phenol. The generation of OH did not influence the [3H]nitrendipine binding; also other oxidative agents (H2O2 and HClO4) did not modify this binding. Therefore the reduction in [3H]nitrendipine binding sites is not attributable to generic oxidative stress but to the formation of carbon centered radicals.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzene Derivatives / pharmacology*
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Butylated Hydroxytoluene / pharmacology
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Calcium Channels / drug effects
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Calcium Channels / metabolism*
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Calcium Channels, L-Type
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Cell Membrane / metabolism
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Down-Regulation
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Electron Spin Resonance Spectroscopy
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Free Radicals
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Hydrogen Peroxide / pharmacology
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Kinetics
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Male
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Myocardium / metabolism*
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Nitrendipine / metabolism*
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Oxidants / pharmacology
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Oxidative Stress
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Perchlorates / pharmacology
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Rats
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Rats, Sprague-Dawley
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Sodium Compounds / pharmacology
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Superoxides / metabolism
Substances
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Benzene Derivatives
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Calcium Channels
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Calcium Channels, L-Type
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Free Radicals
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Oxidants
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Perchlorates
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Sodium Compounds
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Superoxides
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Butylated Hydroxytoluene
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sodium perchlorate
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Nitrendipine
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Hydrogen Peroxide
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cumene hydroperoxide