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Molecular Pharmacology, Vol 3, 509-515, Copyright © 1967 by the American Society for Pharmacology and Experimental Therapeutics
1 Department of Pharmacology, Baylor University College of Medicine,
Texas Medical Center, Houston, Texas 77025
Previously reported beneficial effects of dipyridamole on "damaged" mitochondria have not been confirmed in these experiments. Dipyridamole, in fact, has specific stimulatory or inhibitory effects on mitochondrial respiration depending on which segment of the electron transport chain is predominant. It is postulated that dipyridamole inhibits respiration by accepting electrons from NADH, thus competing with the main electron transport pathway for electrons. The drug is also capable of interacting with a highenergy intermediate when succinate is the substrate, resulting in an "uncoupling-like" action.
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ACKNOWLEDGMENTS
This investigation was supported by grants
from the USPHS (HE 07906-05; HE 05435-07,
P.8) and by the National Science Foundation
(GB 4070). Support from the Texas and Houston
Heart Associations is also acknowledged. Dr.
Schwartz is a recipient of a USPHS Career
Research Development Award (K3HE 11, 875-03).