Abstract
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.
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