atrial natriuretic peptide regulates ca2+ channel in early developmental cardiomyocytes心房利钠肽调节钙离子通道在发育早期心肌细胞.pdfVIP

atrial natriuretic peptide regulates ca2+ channel in early developmental cardiomyocytes心房利钠肽调节钙离子通道在发育早期心肌细胞.pdf

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atrialnatriureticpeptideregulatesca2channelinearlydevelopmentalcardiomyocytes心房利钠肽调节钙离子通道在发育早期心肌细胞

Atrial Natriuretic Peptide Regulates Ca2+ Channel in Early Developmental Cardiomyocytes 1 1 1 1 1 2 ¨ Lin Miao , Min Wang , Wen-Xuan Yin , Qi Yuan , Ying-Xiao Chen , Bernd Fleischmann , Jurgen 3 1 Hescheler *, Guangju Ji * 1 National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China, 2 Institute of Physiology, University of Bonn, Bonn, ¨ Germany, 3 Institute of Neurophysiology, University of Cologne, Koln, Germany Abstract Background: Cardiomyocytes derived from murine embryonic stem (ES) cells possess various membrane currents and signaling cascades link to that of embryonic hearts. The role of atrial natriuretic peptide (ANP) in regulation of membrane potentials and Ca2+ currents has not been investigated in developmental cardiomyocytes. Methodology/Principal Findings: We investigated the role of ANP in regulating L-type Ca2+ channel current (ICaL) in different developmental stages of cardiomyocytes derived from ES cells. ANP decreased the frequency of action potentials (APs) in early developmental stage (EDS) cardiomyocytes, embryonic bodies (EB) as well as whole embryo hearts. ANP exerted an inhibitory effect on basal ICaL in about 70% EDS cardiomyocytes tested but only in about 30% late developmental stage (LDS) cells. However, after stimulation of ICaL by isoproterenol (ISO) in LDS cells, ANP inhibited the response in about 70% cells. The depression of ICaL induced by ANP was not affected by either Nv, Nitro-L-Arginine methyl ester (L-NAME), a nitric oxide synthet

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