Linked Life Data

18177588

Source:http://linkedlifedata.com/resource/pubmed/id/18177588

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-1-7
pubmed:abstractText
There is no question about the contributory risk of hypertension in morbidity and mortality from cardiovascular (CV) disease and chronic kidney disease (CKD). Another independent risk factor for CV disease and CKD is proteinuria, which is most commonly caused by dysfunction of the kidney glomerular filter, in particular of the podocyte. Podocytes are highly differentiated pericyte-like cells that are essential to normal kidney function. Moreover, loss of podocytes is a hallmark of diabetic and nondiabetic progressive CKD. Recent data point to an important role for the renin-angiotensin system (RAS) and calcium signaling in the structural and functional integrity of podocytes. Given this scenario, it is desirable to treat hypertension with agents targeting the RAS, such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (Ang II) type 1-receptor blockers (ARB). These agents have proven effects on lowering blood pressure (BP) and can reduce podocyte injury. Here we review the dual effects of RAS blockade on BP and on podocyte function and emphasize BP-dependent and BP-independent effects of this regimen.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1522-6417
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
403-8
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Dual effects of RAS blockade on blood pressure and podocyte function.
pubmed:affiliation
Division of Nephrology, Program in Glomerular Disease, Massachusetts General Hospital and Harvard Medical School, CNY-149, 13th Street, Suite 8214, Boston, MA 02129, USA. jreiser@partners.org
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural