Restoration of nitric oxide function in human hyperlipidaemia, congestive heart failure and liver cirrhosis.
1. There is accumulating evidence for a range of abnormalities in the nitric oxide (NO) signalling cascade in human cardiovascular disorders. 2. In the present review we assess the literature detailing such evidence in early (hyperlipidaemia) and end-stage (heart failure) disease, with emphasis on the mechanisms by which the disturbances are thought to occur. 3. Strategies for the correction of disturbed NO signalling in these states are reviewed and include both prescribed pharmacological interventions, such as lipid-lowering therapy and novel uses of angiotensin-converting enzyme inhibitors, as well as non-pharmacological interventions, such as exercise and dietary supplementation with L-arginine and n-3 polyunsaturated fatty acids. 4. In addition to a decreased production/function of NO, the possible detrimental effects of a chronic elevation in NO production in patients with liver cirrhosis, together with a novel use of antibiotics to correct this perturbation, is outlined.
Chin-Dusting
J P
JP
Alfred and Baker Medical Unit, Baker Medical Research Institute, Victoria, Australia. jaye.chin@baker.edu.au
Kaye
D M
DM
D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D006949:Hyperlipidemias / Q000503:physiopathology*; D008103:Liver Cirrhosis / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
D009569:Nitric Oxide