20 Result(s)
within
Michael E Mendelsohn
-
Article
Familial Hypertrophic Cardiomyopathy Mice Display Gender Differences in Electrophysiological Abnormalities
Genetically-manipulated mice harboring an α-myosin heavy chain Arg403Gln missense mutation (α-MHC 403/+ ) display a phenotype characteristic of familial hypertrophic cardiomyopathy (FHC). Male and female (30±8...
-
Article
Estrogen inhibits the vascular injury response in estrogen receptor α-deficient mice
The atheroprotective effects of estrogen in women are well recognized1, but the underlying mechanisms responsible are not well understood. Blood vessel cells express the classic estrogen receptor, ERα (ref. 2—6),...
-
Article
Establishment of an Immortalized Fetal Intrapulmonary Artery Endothelial Cell Line • 131
-
Article
Role of Estrogen Receptor Alpha in the Nongenomic Activation of Endothelial Nitric Oxide Synthase by Estradiol • 93
-
Article
Molecular Biology of Human Arrhythmias: Implications for the Clinical Electrophysiologist
-
Article
Differential Roles of Estrogen Receptors Alpha and Beta in the Nongenomic Activation of Endothelial Nitric Oxide Synthase by Estradiol
-
Article
Estrogen Receptors and eNOS are Colocalized as Components of a Signaling Module on the Plasma Membrane of Endothelial Cells
-
Article
High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase
Atherosclerosis is the primary cause of cardiovascular disease, and the risk for atherosclerosis is inversely proportional to circulating levels of high-density lipoprotein (HDL) cholesterol. However, the mech...
-
Article
Regulator of G-protein signaling-2 mediates vascular smooth muscle relaxation and blood pressure
Nitric oxide (NO) inhibits vascular contraction by activating cGMP-dependent protein kinase I-α (PKGI-α), which causes dephosphorylation of myosin light chain (MLC) and vascular smooth muscle relaxation. Here ...
-
Article
Correction: Corrigendum: Regulator of G-protein signaling-2 mediates vascular smooth muscle relaxation and blood pressure
Nat. Med. 9, 1506–1512 (2003) The names of authors K. Mary Tang and Guang-rong Wang were spelled incorrectly.
-
Article
Viagra: now mending hearts
Viagra operates by increasing the levels of cGMP in target cells. This same mechanism underlies a newly discovered action of the drug in mouse hearts: counteracting hypertrophy (pages 214–222
-
Article
Open AccessCreation and characterization of mice with selective mutation of the cyclic GMP-dependent protein kinase I interaction domain
-
Article
Open AccessIn vivo evidence that cyclic GMP-dependent protein kinase G type I α mediates an anti-hypertrophic pathway in the heart
-
Article
Open AccessRegulation of cardiovascular physiology by cyclic GMP-dependent protein kinase Iα
-
Article
Gender differences in the cardiovascular effect of sex hormones
Sex differences in vascular biology are determined not only by gender-related differences in sex steroid levels, but also by gender-specific tissue and cellular differences that mediate sex-specific responses ...
-
Article
Open AccessCyclic GMP-dependent protein kinase regulation of airway smooth muscle in asthma
-
Article
Open AccessLittle ROCK is a ROCK1 pseudogene expressed in human smooth muscle cells
Sequencing of the human genome has identified numerous chromosome copy number additions and subtractions that include stable partial gene duplications and pseudogenes that when not properly annotated can inter...
-
Article
Open AccessSmooth muscle cell specific deletion of the PKGIα target RGS2 induces vascular dysfunction and hypertension
-
Article
Open AccessProtein kinase G I alpha activates an anti-remodeling signaling pathway in the heart via an interaction with the MAPKKK mixed lineage kinase 3
-
Article
Direct regulation of blood pressure by smooth muscle cell mineralocorticoid receptors
The mineralocorticoid receptor, targeted by drugs commonly used to treat hypertension, is generally thought to contribute to hypertension by altering kidney function. Using mice lacking the mineralocorticoid r...
