Mechanisms of Disease: the role of GRK4 in the etiology of essential hypertension and salt sensitivity
Robin A Felder* and Pedro A Jose
Correspondence *Department of Pathology, Post Office Box 800403, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA
Email rfelder@virginia.edu
Are polymorphisms of the G protein-coupled receptor kinase GRK4 the key to developing new tools for the diagnosis and management of essential hypertension? Here, Felder and Jose explore the therapeutic potential of manipulating this protein, which regulates the activity of the dopamine-1 receptor. The role of GRK4 is set in the context of the contributions of the dopaminergic and renin–angiotensin systems to the pathogenesis of hypertension.
Full text of this article is available with one of the following:
- Membership of the International Society of Nephrology. If already a member, please login. If not please join the Society now
- Personal subscription Purchase your own personal subscription to this journal. Already a subscriber? Please login for immediate access.
- 7 day single article pass for US$32 In order to purchase this article you must be a registered user. Please register or login above.
- Site licence Learn more about institutional site licences
Current Subscribers
Please log in to access the full text article using the login box at the top of the page.
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
RESEARCH
D1 dopamine receptor hyperphosphorylation in renal proximal tubules in hypertensionKidney International Original Article
D1 dopamine receptor hyperphosphorylation in renal proximal tubules in hypertensionKidney International Original Article
Desensitization of human renal D1 dopamine receptors by G protein-coupled receptor kinase 4Kidney International Original Article
Primary renal abnormalities in hereditary hypertensionKidney International Original Article
See all 33 matches for Research