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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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Angiotensin II Activates Matrix Metalloproteinase Type II and Mimics Age-Associated Carotid Arterial Remodeling in Young Rats

TL;DR: Ang II-induced effects on MMP2, transforming growth factor-beta1, collagen, and VSMCs are central to the arterial remodeling that accompanies advancing age.
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Variations in the G6PC2/ABCB11 genomic region are associated with fasting glucose levels.

TL;DR: The results in combination with data reported in the literature suggest that G6PC2, a glucose-6-phosphatase almost exclusively expressed in pancreatic islet cells, may underlie variation in fasting glucose, though it is possible that ABCB11, which is expressed primarily in liver, may also contribute to such variation.
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Is digoxin really important in treatment of compensated heart failure?. A placebo-controlled crossover study in patients with sinus rhythm

TL;DR: The results indicate that long-term digoxin therapy has only a minor effect on cardiac performance that is without apparent clinical importance in a representative population of ambulatory patients treated with cardiac glycosides.
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Kappa and delta opioid receptor stimulation affects cardiac myocyte function and Ca2+ release from an intracellular pool in myocytes and neurons.

TL;DR: The hypothesis that delta and kappa opioid receptor stimulation may cause sarcoplasmic reticulum Ca2+ depletion is tested and it is shown that this effect is coupled to phosphatidylinositol turnover and, at least in part, may be due to sarcoplasmsic retICulum Ca 2+ depletion.
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Role of inflammation in the pathogenesis of arterial stiffness.

TL;DR: There is rationale for targeting specific inflammatory pathways involved in arterial stiffness in the development of future drugs, including drugs that block the activation of the RAS system, among the major classes of anti hypertensive drugs.