-
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...
-
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
Open AccessCyclic GMP-dependent protein kinase regulation of airway smooth muscle in asthma
-
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
Open AccessCreation and characterization of mice with selective mutation of the cyclic GMP-dependent protein kinase I interaction domain
-
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
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
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
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
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),...