Torres-Jácome Julián, Tejeda-Chávez Hector R, Rodríguez-Menchaca Aldo A, Sánchez-Chapula José A, Navarro-Polanco Ricardo A
Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, Colima, Col. México.
J Cardiovasc Pharmacol. 2006 May;47(5):656-62. doi: 10.1097/01.fjc.0000211753.47067.cc.
The D3-dopaminergic agonist (+/-) 7-hydroxy-dipropylaminotetralin (7-OH-DPAT) prolonged cycle length and action potential duration, depolarized maximum diastolic potential, and reduced the upstroke velocity of the action potential of rabbit sinoatrial node cells. These effects were not mediated by D3-dopaminergic receptors. In cat Purkinje fibers, the drug increased action potential duration. In voltage-clamped cat ventricular myocytes, 7-OH-DPAT blocked the rapid component of the delayed rectifier potassium current, IKr. This effect was corroborated in experiments studying the effect of the drug on human Ether-a-go-go-related Gene channels expressed in Xenopus oocytes and in HEK293 cells. We conclude that the direct electrophysiologic effects of 7-OH-DPAT on cardiac tissues are caused by the blockade of the rapid component of the delayed rectifier potassium current, IKr.
D3-多巴胺能激动剂(±)7-羟基-二丙基氨基四氢萘(7-OH-DPAT)可延长兔窦房结细胞的周期长度和动作电位时程,使最大舒张电位去极化,并降低动作电位的上升速度。这些作用并非由D3-多巴胺能受体介导。在猫浦肯野纤维中,该药物可增加动作电位时程。在电压钳制的猫心室肌细胞中,7-OH-DPAT可阻断延迟整流钾电流IKr的快速成分。在研究该药物对非洲爪蟾卵母细胞和HEK293细胞中表达的人类醚-去极化相关基因通道影响的实验中,这一作用得到了证实。我们得出结论,7-OH-DPAT对心脏组织的直接电生理作用是由延迟整流钾电流IKr的快速成分被阻断所致。