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Biochemical aspects of the mechanism of action of antiarrhythmic drugs on mitochondria. VII. Effect on energy‐linked reactions and on membrane potential
Author(s) -
Klüppel Maria Lúcia Wambier,
Borba Hélcio Resende,
Silveira Orieta,
Lopes Luiz Carlos Vieira,
De Paiva Campello Annibal
Publication year - 1986
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290040410
Subject(s) - submitochondrial particle , propranolol , chemistry , membrane potential , mitochondrion , mechanism of action , atpase , membrane , succinate dehydrogenase , pharmacology , inner mitochondrial membrane , enzyme , chemiosmosis , biochemistry , biophysics , atp synthase , biology , in vitro , endocrinology
Effects of the antiarrhythmic drugs (propranolol, perhexiline maleate, lidoflazine and iproveratril) on energy‐linked reactions and on membrane potential were studied. Propranolol, perhexiline maleate and lidoflazine inhibit the ATPase activity of undamaged and broken mitochondria, and of submitochondrial particles. All drugs are inhibitors of either ATP‐driven or of succinate‐driven reduction of NADP + . The antiarrhythmics promote a decrease in the membrane potential upon energization of the mitochondrial membrane by α‐ketoglutarate, succinate, or ATP. It was suggested that these drugs have a primary action on the mitochondrial membrane, thus altering the activities of membrane proteins (channels and enzymes).