scispace - formally typeset
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
More filters
Journal ArticleDOI

Coupling of beta2-adrenoceptor to Gi proteins and its physiological relevance in murine cardiac myocytes.

TL;DR: Beta2ARs in murine cardiac myocytes couple to concurrent Gs and Gi signaling, resulting in null inotropic response, unless the Gi signaling is inhibited, and results suggest that PTX-sensitive G proteins are responsible for the unresponsiveness of mouse heart to agonist-induced beta2AR stimulation.
Journal ArticleDOI

AGEMAP: a gene expression database for aging in mice.

TL;DR: The AGEMAP (Atlas of Gene Expression in Mouse Aging Project) gene expression database is presented, which is a resource that catalogs changes in gene expression as a function of age in mice and finds great heterogeneity in the amount of transcriptional changes with age in different tissues.
Journal ArticleDOI

Aortic Stiffness Is Associated With Visceral Adiposity in Older Adults Enrolled in the Study of Health, Aging, and Body Composition

TL;DR: Among older adults, higher levels of visceral fat are associated with greater aortic stiffness as measured by pulse wave velocity, and this association was consistent across tertiles of body weight.
Journal Article

Functional coupling of the beta 2-adrenoceptor to a pertussis toxin-sensitive G protein in cardiac myocytes.

TL;DR: It is shown that pertussis toxin (PTX) pretreatment specifically potentiates the responses of rat heart cells to beta 2AR but not beta 1AR stimulation, and that the Gs-coupled beta 2 AR can simultaneously activate a pathway that leads to functional inhibition in cardiac cells via a PTX-sensitive G protein.