Steady endothelial nitric oxide synthase expression in heart failure.
BACKGROUND
Vascular nitric oxide (NO)-mediated vasodilation is reduced in the limb vasculature of patients with chronic heart failure. Depressed gene expression of vascular endothelial NO synthase has been reported in experimental models of heart failure. We sought to investigate endothelial NO synthase (eNOS) mRNA expression in the skeletal muscle vasculature of patients with chronic heart failure (CHF) and in controls.


RESULTS
Transcript levels for eNOS were measured and normalized to von Willebrand factor gene expression level, in samples of skeletal muscle from patients with CHF (n = 20) and healthy subjects (n = 7). CHF was not associated with a decrease in eNOS expression. There was a trend towards an increased expression in NYHA class IV patients. Similar results were found when normalized to GAPDH mRNA levels.


CONCLUSIONS
Vascular endothelial dysfunction that is observed in patients with severe heart failure does not appear to be related to a specific decrease in the expression of the gene encoding for endothelial NOS.
Ennezat
Pierre V
PV
Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx, New York, USA. ennezat@yahoo.com
Van Belle
Eric
E
Asseman
Philippe
P
Cohen-Solal
Alain
A
Evans
Todd
T
Lejemtel
Thierry H
TH
D000368:Aged; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D006333:Heart Failure / Q000201:enzymology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018709:Statistics, Nonparametric
D052250:Nitric Oxide Synthase Type III