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
Adenovirus-Mediated VEGF121 Gene Transfer Stimulates Angiogenesis in Normoperfused Skeletal Muscle and Preserves Tissue Perfusion After Induction of Ischemia
Luis Henrique W. Gowdak,Lioubov Poliakova,Xiaotong Wang,Imre Kovesdi,Kenneth W. Fishbein,Antonella Zacheo,Roberta Palumbo,Stefania Straino,Costanza Emanueli,Massimiliano Marrocco-Trischitta,Edward G. Lakatta,Piero Anversa,Richard G. Spencer,Mark I. Talan,Maurizio C. Capogrossi +14 more
TL;DR: IM administration of AdCMV.VEGF(121) stimulates angiogenesis in normoperfused skeletal muscles, and the newly formed vessels preserve TP after induction of ischemia.
Journal ArticleDOI
Scattered-light intensity fluctuations in diastolic rat cardiac muscle caused by spontaneous Ca++-dependent cellular mechanical oscillations.
Michael D. Stern,Michael D. Stern,A A Kort,A A Kort,Gopal Bhatnagar,Gopal Bhatnagar,Edward G. Lakatta +6 more
TL;DR: It is inferred that mechanical oscillations caused by spontaneous Ca++-induced Ca++ release from the SR occur in intact nonstimulated cardiac muscle even in the absence of Ca++ overload and are the principle cause of SLIF, and that myoplasmic [Ca++] in "resting" muscle is not in a microscopic steady state.
Journal ArticleDOI
Synchronous occurrence of spontaneous localized calcium release from the sarcoplasmic reticulum generates action potentials in rat cardiac ventricular myocytes at normal resting membrane potential.
TL;DR: The synchronous occurrence of multifocal localized increases in cytosolic Ca2+ due to spontaneousCa2+ release from the sarcoplasmic reticulum within ventricular myocytes is a mechanism for "abnormal automaticity."
Journal ArticleDOI
Age associated changes in membrane currents in rat ventricular myocytes
K. E. Walker,K. E. Walker,K. E. Walker,Edward G. Lakatta,Edward G. Lakatta,Edward G. Lakatta,Steven R. Houser,Steven R. Houser,Steven R. Houser +8 more
TL;DR: ICa density is maintained in senescence; ICa inactivation, however, is slowed; ITO channels appear to retain normal function through the aging process but overall there is a reduced channel density.
Journal ArticleDOI
Enhanced Gi Signaling Selectively Negates β2-Adrenergic Receptor (AR)– but Not β1-AR–Mediated Positive Inotropic Effect in Myocytes From Failing Rat Hearts
Rui-Ping Xiao,Sheng Jun Zhang,Khalid Chakir,Pavel Avdonin,Weizhong Zhu,Richard A. Bond,C. William Balke,C. William Balke,Edward G. Lakatta,Heping Cheng +9 more
TL;DR: It is concluded that enhanced Gi signaling is selectively involved in the dysfunction of &bgr;2- but not &b gr;1-AR in failing SHR hearts and that disruption of Gi signaling by PTX or selective activation of & bgr; 2-AR/Gs signaling by fenoterol restores the blunted &b Gr;2;-AR contractile response in the failing heart.