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Melatonin and its analogs potentiate the nifedipine‐sensitive high‐voltage‐activated calcium current in the chick embryonic heart cells
Author(s) -
Mei Y.A.,
Lee P.P.N.,
Wei H.,
Zhang Z.H.,
Pang S.F.
Publication year - 2001
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1034/j.1600-079x.2001.300102.x
Subject(s) - melatonin , endocrinology , medicine , calcium , nifedipine , voltage dependent calcium channel , calcium channel , myocyte , biology , t type calcium channel , contractility , melatonin receptor , patch clamp , chemistry , receptor
Effects of melatonin and its analogs on the voltage‐activated calcium current of embryonic chick ventricular cardiomyocytes were investigated. Myocytes were dissociated from 14‐ to 16‐day‐old chicks (yellow Red Rob) embryonic hearts and cultured for 2–3 days. Calcium currents were studied by the patch‐clamp technique. Whole‐cell current recording showed nifedipine‐sensitive, high‐voltage‐activated L‐type calcium current inactivated in 70–100 ms during the voltage step period of 200 ms. There was no evidence of low‐voltage‐activated T‐type calcium channels. Melatonin (ejected solution: 50 μmol/L melatonin; concentration at the vicinity of recording cell: about 1–5 μmol/L melatonin) and its analogs, 2‐iodomelatonin and 2‐iodo‐n‐butanol‐5‐methoxytryptamine, significantly increased the amplitude of the calcium current by 42–62%. The effect of melatonin on the L‐type calcium current was not desensitised by repeated melatonin treatment. Our results suggest a specific melatonin receptor‐mediated action on the calcium channel of the embryonic chick myocyte. The melatonin‐induced increase in high‐voltage calcium current may increase myocyte contractility and enhance cardiac output. A regulatory role of melatonin on the chick cardiac function should be further considered.