Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Statins and the role of nitric oxide in chronic heart failure

Item Type:Article
Title:Statins and the role of nitric oxide in chronic heart failure
Creators Name:von Haehling, S. and Anker, S.D. and Bassenge, E.
Abstract:Endothelial dysfunction plays an important role in a number of cardiovascular diseases. An important pathogenetic factor for the development of endothelial dysfunction is lack of nitric oxide (NO), which is a potent endothelium-derived vasodilating substance. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins), originally designed to lower plasma cholesterol levels, seem to ameliorate endothelial dysfunction by a mechanism so far only partly understood. However, statins increase nitric oxide synthase activity. It has been speculated that this and other "side effects" of statin treatment are due to inhibition of Rho, an intracellular signalling protein that initiates Rho kinase transcription. Moreover, statins possess anti-inflammatory characteristics. Some statins have proven to lower plasma levels of C-reactive protein, which is induced by pro-inflammatory cytokines. Other statins have been demonstrated to directly inhibit pro-inflammatory cytokine induction. Finally, some data suggest that statins might be able to counterbalance an increased production of oxygen free radicals. Since chronic heart failure is accompanied not only by endothelial dysfunction, but also by pro-inflammatory cytokine activation and enhanced formation of oxygen free radicals, it is tempting to speculate that statins might be an ideal candidate to treat certain features of this disease. The doses needed to achieve the desired effects might be much lower than those needed to treat hypercholesterolemia.
Keywords:Chronic Heart Failure, Endothelial Dysfunction, Nitric Oxide, Statin
Source:Heart Failure Reviews
ISSN:1382-4147
Volume:8
Number:1
Page Range:99-106
Date:1 January 2003
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library