Linked Life Data

19893565

Source:http://linkedlifedata.com/resource/pubmed/id/19893565

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-1-5
pubmed:abstractText
Renin inhibitors, similar to all renin-angiotensin system (RAS) blockers, increase the plasma concentration of renin because they attenuate the negative feedback effect of angiotensin (Ang) II on renin release. The increase in renin has been suggested to be higher than that during other types of RAS blockade. This could potentially limit the effectiveness of renin inhibition, either because Ang II generation might occur again ('Ang II escape'), possibly even at the levels above baseline, as has been described before for angiotensin-converting enzyme inhibitors, or because high levels of renin will stimulate the recently discovered (pro)renin receptor, and thus induce effects in an Ang-independent manner. This review shows first that the cause(s) of the renin increase during treatment with the renin inhibitor aliskiren is the consequence of a combination of factors, including an assay artifact, allowing the detection of prorenin as renin, and a change in renin half-life. When correcting for these phenomena the increase is unlikely to be as excessive as originally thought. The review then critically describes the consequence(s) of such a increase, concluding (i) that an Ang II escape is highly unlikely, given the [aliskiren]/[renin] stoichiometry, and (ii) that renin and prorenin downregulate their receptor (similar to many agonists). On the basis of the latter, one could even speculate that this will be more substantial when the renin and prorenin levels are higher. Thus, from this point of view the larger increase in renin during renin inhibition will cause a stronger reduction in (pro)renin receptor expression, and a greater suppression of (pro)renin receptor-mediated effects than other renin-Ang blockers.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1348-4214
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4-10
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
The increase in renin during renin inhibition: does it result in harmful effects by the (pro)renin receptor?
pubmed:affiliation
Division of Pharmacology, Vascular and Metabolic Diseases, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands. a.danser@erasmusmc.nl
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't