Expression of inducible nitric oxide synthase is increased in patients with heart failure due to ischemic disease

The objective of the present study was to determine the relationship between nitric oxide synthases (NOS) and heart failure in cardiac tissue from patients with and without cardiac decompensation. Right atrial tissue was excised from patients with coronary artery disease (CAD) and left ventricular e...

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Bibliographic Details
Published in:Brazilian journal of medical and biological research 2004-09, Vol.37 (9), p.1313-1320
Main Authors: Ferreiro, C R, Chagas, A C P, Carvalho, M H C, Dantas, A P, Scavone, C, Souza, L C B, Buffolo, E, da Luz, P L
Format: Article
Language:English
Subjects:
Aged
BIOLOGY
Coronary Angiography
Coronary Artery Disease - complications
Coronary Artery Disease - surgery
Female
Gene Expression
Heart Failure - enzymology
Heart Failure - etiology
Humans
Male
MEDICINE, RESEARCH & EXPERIMENTAL
Middle Aged
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Reverse Transcriptase Polymerase Chain Reaction
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Summary:The objective of the present study was to determine the relationship between nitric oxide synthases (NOS) and heart failure in cardiac tissue from patients with and without cardiac decompensation. Right atrial tissue was excised from patients with coronary artery disease (CAD) and left ventricular ejection fraction (LVEF) 60% (N = 10) during cardiac surgery. NOS activity was measured by the conversion of L-[H(3)]-arginine to L-[H(3)]-citrulline. Gene expression was quantified by the competitive reverse transcription-polymerase chain reaction. Both endothelial NOS (eNOS) activity and expression were significantly reduced in failing hearts compared to non-failing hearts: 0.36 +/- 0.18 vs 1.51 +/- 0.31 pmol mg-1 min-1 (P < 0.0001) and 0.37 +/- 0.08 vs 0.78 +/- 0.09 relative cDNA absorbance at 320 nm (P < 0.0001), respectively. In contrast, inducible NOS (iNOS) activity and expression were significantly higher in failing hearts than in non-failing hearts: 4.00 +/- 0.90 vs 1.54 +/- 0.65 pmol mg-1 min-1 (P < 0.0001) and 2.19 +/- 0.27 vs 1.43 +/- 0.13 cDNA absorbance at 320 nm (P < 0.0001), respectively. We conclude that heart failure down-regulates both eNOS activity and expression in cardiac tissue from patients with LVEF
ISSN:0100-879X
1414-431X
0100-879X
DOI:10.1590/S0100-879X2004000900005