Klüppel M L, Borba H R, Silveira O, Lopes L C, Campello A de P
Cell Biochem Funct. 1986 Oct;4(4):289-96. doi: 10.1002/cbf.290040410.
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 alpha-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).
研究了抗心律失常药物（普萘洛尔、马来酸哌克昔林、利多氟嗪和维拉帕米）对能量偶联反应和膜电位的影响。普萘洛尔、马来酸哌克昔林和利多氟嗪可抑制完整及破碎线粒体以及亚线粒体颗粒的ATP酶活性。所有药物均为ATP驱动或琥珀酸驱动的NADP⁺还原反应的抑制剂。这些抗心律失常药物可促使α-酮戊二酸、琥珀酸或ATP使线粒体膜通电后膜电位降低。有人提出，这些药物对线粒体膜有主要作用，从而改变膜蛋白（通道和酶）的活性。
