E
Edward G. Lakatta
Researcher at National Institutes of Health
Publications - 902
Citations - 95504
Edward G. Lakatta is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Blood pressure & Population. The author has an hindex of 146, co-authored 858 publications receiving 88637 citations. Previous affiliations of Edward G. Lakatta include University of Pittsburgh & University College London.
Papers
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Journal ArticleDOI
Beat to beat Ca2+-dependent regulation of sinoatrial nodal pacemaker cell rate and rhythm
Yael Yaniv,Victor A. Maltsev,Ariel L. Escobar,Harold A. Spurgeon,Bruce D. Ziman,Michael D. Stern,Edward G. Lakatta +6 more
TL;DR: The hypothesis that intracellular Ca(2+) regulates normal SANC automaticity on a beat-to-beat basis is supported.
Journal ArticleDOI
Ca2+/Calmodulin-Dependent Protein Kinase II (CaMKII) Activity and Sinoatrial Nodal Pacemaker Cell Energetics
TL;DR: CaMKII signaling, a crucial element of normal automaticity in rabbit SANC, is also involved in SANC bioenergetics and graded reductions in ATP demand indicate reduced ATP production.
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Long-term low dose dietary resveratrol supplement reduces cardiovascular structural and functional deterioration in chronic heart failure in rats.
TL;DR: It is demonstrated that long-term dietary resveratrol supplement reduces cardiovascular structural and functional deterioration in CHF and improves LV systolic function and AV-coupling in R compared with Control.
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Sustained subthreshold-for-twitch depolarization in rat single ventricular myocytes causes sustained calcium channel activation and sarcoplasmic reticulum calcium release.
TL;DR: It is concluded that when a sustained depolarization does not exceed about -20 mV, the resultant steady, graded contraction is due to SR Ca2+ release graded by a steady ("window") Ca2+, and implies a distinction between the triggering and released Ca2+.
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Ca2 +/calmodulin-activated phosphodiesterase 1A is highly expressed in rabbit cardiac sinoatrial nodal cells and regulates pacemaker function
Yevgeniya O. Lukyanenko,Antoine Younes,Alexey E. Lyashkov,Alexey E. Lyashkov,Kirill V. Tarasov,Daniel R. Riordon,JoonHo Lee,Syevda Sirenko,Evgeny Kobrinsky,Bruce D. Ziman,Yelena S. Tarasova,Magdalena Juhaszova,Steven J. Sollott,David R. Graham,Edward G. Lakatta +14 more
TL;DR: It is concluded that signaling via cAMP generated by Ca(2+)/CaM-activated AC in SANC lipid raft domains is limited by cAMP degradation by Ca (2+/CaM)-activated PDE1A in non-lipid raft domains.