Bufalin exerts negative inotropic effects and inhibits L-type calcium channels in rat ventricular myocytes, providing a potential cellular mechanism for its cardiac effects.
Bufalin's Ca channel effects may reduce contractility; leaves open clinical relevance to Chan Su cardiotoxicity.
Bufalin is a bufanolide steroid compound in Chan Su. Chan Su is a traditional Chinese medicine prepared from the dried white secretion of the auricular and skin glands of toads and has been used as an oriental drug. However, the effect of bufalin on cardiac function and its underlying cellular mechanisms remain unclear. Here, we explore the cellular mechanisms of bufalin on myocardial protection via the whole‐cell patch‐clamp recording and video‐based edge detection system. Exposure to bufalin resulted in a concentration‐dependent blockade of I C a‐L , with the half‐maximal inhibitory concentration ( IC 50 ) of 60 μ m and the maximal inhibitory effect of 71.50 ± 2.67%. Bufalin at 100 μ m reduced cell shortening by 33.83 ± 4.01%. Bufalin restrained L‐type Ca 2+ channels conductance, and contractility in rat ventricular myocytes. Thus, the protective effects of bufalin on the heart may be determined by the inhibitory effect on I C a‐L and the negative inotropic action caused by the decrease of intracellular Ca 2+ in rat myocardial cells.
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Song et al. (2017) studied this question.
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