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Atrioventricular conduction and arrhythmias at the initiation of beating in embryonic mouse hearts
Author(s) -
Chen Fuhua,
De Diego Carlos,
Chang Marvin G.,
McHarg Jennifer L.,
John Scott,
Klitzner Thomas S.,
Weiss James N.
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22319
Subject(s) - endoplasmic reticulum , embryonic heart , nifedipine , tetrodotoxin , medicine , biology , intracellular , calcium , channel blocker , membrane potential , adenosine , ryanodine receptor , anatomy , endocrinology , embryonic stem cell , cardiology , biophysics , microbiology and biotechnology , biochemistry , gene
To investigate cardiac physiology at the onset of heart beating in embryonic mouse hearts, we performed optical imaging of membrane potential (Vm) and/or intracellular calcium (Ca i ). Action potentials and Ca i transients were detected in ∼50% of mouse embryo hearts at E8.5, but in all hearts at E9.0, indicating that beating typically starts between E8–E9. Beating was eliminated by Ca channel blocker nifedipine and the I f blocker ZD7288, unaffected by tetrodotoxin and only mildly depressed by disabling sarcoplasmic (SR) and endoplasmic (ER) reticulum Ca cycling. From E8.5 to E10, conduction velocity increased from 0.2–1 mm/s to >5 mm/s in first ventricular and then atrial tissue, while remaining slow in other areas. Arrhythmias included atrioventricular reentry induced by adenosine. In summary, at the onset of beating, I f ‐dependent pacemaking drives both AP propagation and Ca i transient generation through activation of voltage‐dependent Ca channels. Na channels and intracellular Ca cycling have minor roles. Developmental Dynamics 239:1941–1949, 2010. © 2010 Wiley‐Liss, Inc.