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.
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Journal ArticleDOI
Hormone Replacement Therapy and Longitudinal Changes in Blood Pressure in Postmenopausal Women
Angelo Scuteri,Angelo Jose Goncalves Bos,Larry J. Brant,Laura A. Talbot,Edward G. Lakatta,Jerome L. Fleg +5 more
TL;DR: The hypothesis that HRT may be associated with a lesser longitudinal increase in blood pressure in postmenopausal women was tested and whether the association between HRT and blood pressure changes over time differs as a function of the age at which HRT is initiated was investigated.
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Calpain-1 Regulation of Matrix Metalloproteinase 2 Activity in Vascular Smooth Muscle Cells Facilitates Age-Associated Aortic Wall Calcification and Fibrosis
Liqun Jiang,Jing Zhang,Robert E. Monticone,Richard Telljohann,James Wu,Mingyi Wang,Edward G. Lakatta +6 more
TL;DR: Calpain-1 is established as a novel molecular candidate to retard age-associated extracellular matrix remodeling and its attendant risk for hypertension and atherosclerosis.
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From two competing oscillators to one coupled-clock pacemaker cell system
TL;DR: Theoretical and experimental evidence has mounted to indicate that this clock “crosstalk” operates on a beat-to-beat basis and determines both the AP firing rate and rhythm.
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Mechanical properties of myocardium from hypertrophied rat hearts. A comparison between hypertrophy induced by senescence and by aortic banding.
TL;DR: The findings suggest that a portion of the mechanical property alterations seen in the senescent heart are due to the underlying hypertrophy, however, thehypertrophy produced by mechanical loading of the LV cannot explain all of the senescence changes.
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Ryanodine releases calcium from sarcoplasmic reticulum in calcium-tolerant rat cardiac myocytes.
TL;DR: The hypothesis tested in this study is that ryanodine depletes sarcoplasmic reticulum (s.r.) Ca2+ loading in suspensions of single adult rat cardiac myocytes by effecting Ca 2+ release into the myoplasm resulting in an increase in myoplasmsic free [Ca2+] ([Ca2-]i).