title: Contribution of sarcoplasmic reticulum Ca²+ release and Ca²+ transporters on sarcolemmal channels to Ca²+ transient in fetal mouse heart.
abstract: Sarcoplasmic reticulum (SR) Ca release has been shown not to be the predominant mechanism responsible for excitation-contraction (E-C) coupling in fetal myocytes. However, most of the studies have been conducted either on primary cultures or acutely isolated cells, in which an apparent reduction of ryanodine receptor density have been reported. We aimed to elucidate the contribution of SR Ca release and Ca transporters on sarcolemmal channels to Ca transients in fetal mouse whole hearts. On embryonic day 13.5, ryanodine significantly reduced the amplitude of the Ca transient to 27.2 ± 4.4% of the control, and both nickel and SEA0400 significantly prolonged the time to peak from 84 ± 2 ms to 140 ± 5 ms and 129 ± 6 ms, respectively, whereas nifedipine did not alter it. Therefore, at early fetal stages, SR Ca release should be an important component of E-C coupling, and T-type Ca channel and reverse mode sodium-calcium exchanger (NCX)-mediated SR Ca release could be the predominant contributors. Using embryonic mouse cultured cardiomyocytes, we showed that both nifedipine and nickel inhibited the ability of NCX to extrude Ca from the cytosol. From these results, we propose a novel idea concerning E-C coupling in immature heart.
authors.affiliation: Department of Pediatrics, National Defense Medical College, Tokorozawa, Saitama 359-8513, Japan. ishiwata@ndmc.ac.jp
authors.forename: Mari
authors.initials: M
authors.lastname: Takizawa
authors.forename: Takahiro
authors.initials: T
authors.lastname: Ishiwata
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Kawamura
authors.forename: Takashi
authors.initials: T
authors.lastname: Kanai
authors.forename: Takayuki
authors.initials: T
authors.lastname: Kurokawa
authors.forename: Mitsunori
authors.initials: M
authors.lastname: Nishiyama
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Ishida
authors.forename: Yuh
authors.initials: Y
authors.lastname: Asano
authors.forename: Shigeaki
authors.initials: S
authors.lastname: Nonoyama
mesh_terms: D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000378:metabolism; D002478:Cells, Cultured; D005318:Fetal Heart / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D009200:Myocardial Contraction / Q000502:physiology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D009532:Nickel / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D019831:Sodium-Calcium Exchanger / Q000378:metabolism
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D019837:Ryanodine Receptor Calcium Release Channel; D019831:Sodium-Calcium Exchanger; D002110:Caffeine; D009532:Nickel; D009543:Nifedipine; D002118:Calcium