Original Article

Inhibitory effects of serotonin on transient outward potassium current in rat ventricular myocytes.

Authors: Ming-Gao ZHAO, Qi-Bing MEI, Yan-Feng ZHANG, Bing XING, Xiao-Qiang LI, Yi CUI

Abstract

AIM: To study the effects of serotonin (5-hydroxy-tryptamine, 5-HT) on transient
outward potassium current (I(to)) and elucidate its mechanism in rat ventricular
myocytes.
METHODS: I(to) was recorded using the conventional whole cell patch-clamp
techniques.
RESULTS: I(to) density in normal myocytes was similar to that in
norepinephrine-induced hypertrophic myocytes. 5-HT depressed I(to) in a
concentration-dependent manner with the half-maximal inhibitory concentration of
(40+/-5) micromol/L and (38+/-7) micromol/L in normal and hypertrophic
ventricular myocytes respectively. Mianserin (5-HT2 receptor antagonist),
compound 48/80 (phospholipase C antagonist), and chelerythrine chloride (protein
kinase C antagonist) reversed the inhibitory effects of 5-HT on I(to), while
phorbol 12-myristate 13-acetate (protein kinase C agonist) enhanced the
inhibitory effect of 5-HT on I(to) in normal myocytes.
CONCLUSION: 5-HT markedly inhibits I(to) in rat ventricular myocytes. The
putative signal pathway is that 5-HT activates phospholipase C, which causes
inositol phospholipid hydrolysis. The activation of downstream signal molecule,
protein kinase C, phosphorates substrate target proteins, which leads to
inhibition of I(to) in ventricular myocytes.
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