Carpentier R, Narvarte J, Sanhueza S
Cardiovasc Res. 1977 Jan;11(1):39-46. doi: 10.1093/cvr/11.1.39.
The mechanism of the transient enhancement of the amplitude of the action potential (AAP) induced by harmaline (HME) was studied in rat atria. The results show that HME increases AAP through an enhancement of the slow component responsible for the last part of the upstroke, which overcomes an inhibitory action on the initial fast component. The stimulatory effect on the slow component is mediated through adrenergic beta receptors and normally masks an alpha-dependent depressant effect.
研究了大鼠心房中,harmaline(HME)诱导动作电位幅度(AAP)短暂增强的机制。结果表明,HME通过增强负责动作电位上升支最后部分的慢成分来增加AAP,该慢成分克服了对初始快成分的抑制作用。对慢成分的刺激作用通过肾上腺素能β受体介导,且通常掩盖了α依赖性的抑制作用。