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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.

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Leucine-enkephalin increases the level of inositol (1,4,5) triphosphate and releases calcium from an intracellular pool in rat ventricular cardiac myocytes.

TL;DR: Leu-Enk induces depletion of Ca2+ from the SR by a receptor-mediated mechanism which appears to involve an increase in the intracellular level of Ins (1,4,5) P3.
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Endogenous bufadienolide mediates pressor response to ethanol withdrawal in rats

TL;DR: In vivo administration of anti-MBG antibody to rats prevented withdrawal-induced BP elevation, and may link mechanisms of ethanol dependence and hypertension.
Posted ContentDOI

Genetic analysis of over one million people identifies 535 novel loci for blood pressure

Evangelos Evangelou, +315 more
- 11 Oct 2017 - 
TL;DR: This work identifies 535 novel blood pressure loci that not only offer new biological insights into blood pressure regulation but also reveal shared loci influencing lifestyle exposures that offer the potential for a precision medicine strategy for future cardiovascular disease prevention.
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Contribution of spontaneous L-type Ca2+ channel activation to the genesis of Ca2+ sparks in resting cardiac myocytes.

TL;DR: In this paper, the authors used confocal laser scanning microscopy and fluo-4 to visualize local Ca2+ sparks in intact rat ventricular myocytes and found that infrequent and stochastic openings of sarcolemmal L-type channels in resting heart cells contribute significantly to the production of spontaneous Ca 2+ sparks.
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Age Associated Decrease in Intrinsic Action Potential (AP) Firing Rate in Sinoatrial Node Cells is Linked to Deficient Intrinsic cAMP-PKA-Ca2+ Signaling

TL;DR: It is concluded that intrinsic SR Ca2+cycling and its response to PDE inhibition decline with age, and that this decline is linked to the age-associated decrease in IAPFR.