| Is there a future for direct renin inhibitors? | |
| | |
MedLine Citation:
|
PMID: 20380486 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
IMPORTANCE OF THE FIELD: The renin-angiotensin-aldosterone system (RAAS) is a key regulator of blood pressure (BP), as well as volume and electrolytes, in both hypertensive and normotensive individuals. Inappropriate activation of the RAAS is important in hypertension-induced cardiovascular disease (CVD) and chronic kidney disease (CKD). Renin is the rate-limiting step in the RAAS cascade, which makes direct renin inhibitors (DRIs) an attractive target for RAAS suppression and treatment of hypertension. Current regimens using either angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) result in feedback upregulation of renin and aldosterone breakthrough, which contribute to incomplete suppression of the RAAS. Thereby, aliskiren - alone or in combination - might offer a novel therapeutic intervention to improve suppression of the RAAS, with potential to translate to improved CVD and CKD outcomes. AREAS COVERED IN THIS REVIEW: Herein, we present the current state of knowledge of DRIs in the preclinical and clinical realm and their antihypertensive efficacy in relation to cardiovascular and renal risk. Recent clinical trials (2007 - 2009) support the efficacy of aliskiren, and studies suggest the potential for improved CVD and CKD outcomes. WHAT THE READER WILL GAIN: An understanding of the mechanism of action of DRIs and a perspective of recent clinical trials. TAKE HOME MESSAGE: The DRI aliskiren is an effective antihypertensive agent that preliminary data suggests has a beneficial effect in CVD and CKD. Combination of aliskiren with an ACEi or ARB may be better tolerated than the ACEi-ARB combination. Future work is needed to further quantify aliskiren's impact on hard CVD and CKD end points. |
| | |
Authors:
|
Kunal Chaudhary; Ravi Nistala; Adam Whaley-Connell |
Related Documents
:
|
6989756 - Mechanism of enhanced blood pressure rise after reclipping following removal of a renal... 7028466 - Effect of vasopressin blockade on blood pressure regulation during hemorrhage in consci... 962446 - Oral-contraceptive-induced hypertension after adrenalectomy and hypophysectomy. 2474096 - The renin-angiotensin system, the kidney, and hypertension. 4072756 - Ioxaglate versus diatrizoate in selective pulmonary angiography. ii. cardiovascular res... 9814616 - Effect of diaspirin cross-linked hemoglobin on endothelin-1 and blood pressure in acute... |
Publication Detail:
|
Type: Journal Article; Review |
Journal Detail:
|
Title: Expert opinion on investigational drugs Volume: 19 ISSN: 1744-7658 ISO Abbreviation: Expert Opin Investig Drugs Publication Date: 2010 May |
Date Detail:
|
Created Date: 2010-04-20 Completed Date: 2010-07-08 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 9434197 Medline TA: Expert Opin Investig Drugs Country: England |
Other Details:
|
Languages: eng Pagination: 653-61 Citation Subset: IM |
Affiliation:
|
Harry S Truman VA Medical Center, Columbia, MO 65211, USA. chaudharyk@health.missouri.edu |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Amides
/
adverse effects,
pharmacology Animals Antihypertensive Agents / adverse effects, pharmacology* Blood Pressure / drug effects Cardiovascular Diseases / etiology, prevention & control Drug Design Drug Therapy, Combination Fumarates / adverse effects, pharmacology Humans Hypertension / complications, drug therapy*, physiopathology Kidney Diseases / etiology, prevention & control Renin / antagonists & inhibitors* Renin-Angiotensin System / drug effects |
| Chemical | |
Reg. No./Substance:
|
0/Amides; 0/Antihypertensive Agents; 0/Fumarates; 0/aliskiren; EC 3.4.23.15/Renin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Short communication: Human blood dendritic cells are infected separately from monocytes in HIV type ...
Next Document: Adenovirus vaccine immunotherapy targeting WT1-expressing tumors.