PMID- 14984722
OWN - NLM
STAT- MEDLINE
DCOM- 20040921
LR  - 20181130
IS  - 1388-9842 (Print)
IS  - 1388-9842 (Linking)
VI  - 6
IP  - 2
DP  - 2004 Mar 1
TI  - Endothelial dysfunction in congestive heart failure: ACE inhibition vs. 
      angiotensin II antagonism.
PG  - 151-9
AB  - BACKGROUND: Endothelial dysfunction of the vasculature contributes to the 
      elevated peripheral resistance and reduced myocardial perfusion in congestive 
      heart failure (CHF). The present study systematically investigated the effect of 
      angiotensin II (AT(1))- receptor blockade on vascular superoxide (O(2)(-)) 
      production and endothelial dysfunction. METHODS AND RESULTS: Vasodilator 
      responses and O(2)(-) production were determined in aortic rings from Wistar rats 
      with experimental CHF 10 weeks after extensive myocardial infarction and compared 
      with sham-operated animals (Sham). Rats were either treated with placebo (P), 
      with the AT(1)-receptor antagonist Irbesartan (50 mg kg(-1) day(-1)) or with the 
      ACE inhibitor Trandolapril (0.3 mg kg(-1) day(-1)). In CHF-P, 
      endothelium-dependent, acetylcholine-induced relaxation was significantly 
      attenuated compared with Sham-P. Chronic treatment with Trandolapril or 
      Irbesartan significantly improved endothelium-dependent relaxation. Aortic 
      O(2)(-) formation was markedly increased in CHF, and was not significantly 
      affected by Trandolapril treatment, while it was reduced by Irbesartan. eNOS 
      expression was reduced in CHF and normalised by both treatments. CONCLUSION: 
      Endothelial vasomotor function in CHF rats was normalised by long-term treatment 
      with an ACE inhibitor or an AT(1)-antagonist. Reduced aortic eNOS expression was 
      normalised by both treatments, whereas aortic superoxide formation was only 
      reduced by the AT(1)-antagonist Irbesartan.
FAU - Schafer, Andreas
AU  - Schafer A
AD  - Medizinische Klinik der Julius-Maximilians-Universitat Wurzburg, Josef Schneider 
      Str. 2, D-97080 Wurzburg, Germany.
FAU - Fraccarollo, Daniela
AU  - Fraccarollo D
FAU - Tas, Piet
AU  - Tas P
FAU - Schmidt, Isabel
AU  - Schmidt I
FAU - Ertl, Georg
AU  - Ertl G
FAU - Bauersachs, Johann
AU  - Bauersachs J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Eur J Heart Fail
JT  - European journal of heart failure
JID - 100887595
RN  - 0 (Angiotensin Receptor Antagonists)
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Indoles)
RN  - 0 (Tetrazoles)
RN  - 11062-77-4 (Superoxides)
RN  - 1T0N3G9CRC (trandolapril)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.14.13.39 (Nos3 protein, rat)
RN  - J0E2756Z7N (Irbesartan)
SB  - IM
MH  - Analysis of Variance
MH  - *Angiotensin Receptor Antagonists
MH  - Angiotensin-Converting Enzyme Inhibitors/*pharmacology/therapeutic use
MH  - Animals
MH  - Aorta, Thoracic/drug effects/physiopathology
MH  - Biphenyl Compounds/pharmacology/*therapeutic use
MH  - Endothelium, Vascular/*drug effects/metabolism/physiopathology
MH  - Heart Failure/*drug therapy
MH  - Indoles/*pharmacology/therapeutic use
MH  - Irbesartan
MH  - Male
MH  - Nitric Oxide Synthase/biosynthesis
MH  - Nitric Oxide Synthase Type III
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Superoxides/metabolism
MH  - Tetrazoles/pharmacology/*therapeutic use
MH  - Treatment Outcome
MH  - Vasodilation/drug effects
EDAT- 2004/02/27 05:00
MHDA- 2004/09/24 05:00
CRDT- 2004/02/27 05:00
PHST- 2003/06/13 00:00 [received]
PHST- 2003/08/17 00:00 [revised]
PHST- 2003/10/23 00:00 [accepted]
PHST- 2004/02/27 05:00 [pubmed]
PHST- 2004/09/24 05:00 [medline]
PHST- 2004/02/27 05:00 [entrez]
AID - S1388984203002150 [pii]
AID - 10.1016/j.ejheart.2003.10.009 [doi]
PST - ppublish
SO  - Eur J Heart Fail. 2004 Mar 1;6(2):151-9. doi: 10.1016/j.ejheart.2003.10.009.