526 Role of aldosterone in development of secondary coronary endothelial dysfunction in transgenic mice model of heart failure

2006 ◽  
Vol 5 (1) ◽  
pp. 112-112
Author(s):  
L DRELICHARZ ◽  
V KOZLOVSKI ◽  
S CHLOPICKI
Keyword(s):  
Heart Failure ◽  
Endothelial Dysfunction ◽  
Transgenic Mice ◽  
Mice Model ◽  
Coronary Endothelial Dysfunction

scholarly journals A neuroprotective role of aquaporin-4 against other than amyloid β deposition or neuroinflammation in the 5xFAD transgenic mice model.

2020 ◽  
Vol 93 (0) ◽  
pp. 2-P-195
Author(s):  
Yoichiro Abe ◽  
Natsumi Ikegawa ◽  
Minetaka Murakami ◽  
Takumi Tanaka ◽  
Takako Niikura ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Β ◽  
Aquaporin 4 ◽  
Mice Model

Increased inactivation of nitric oxide is involved in coronary endothelial dysfunction in heart failure

2001 ◽  
Vol 280 (1) ◽  
pp. H68-H75 ◽  
Author(s):  
Kenichi Arimura ◽  
Kensuke Egashira ◽  
Ryo Nakamura ◽  
Tomomi Ide ◽  
Hiroyuki Tsutsui ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Endothelial Dysfunction ◽  
Lipid Peroxides ◽  
Canine Model ◽  
Oxygen Free Radical ◽  
Antioxidant Treatment ◽  
Synthesis Inhibitor ◽  
Intracoronary Infusion ◽  
Coronary Endothelial Dysfunction

Recent evidence suggests the possibility that enhanced inactivation of endothelium-derived nitric oxide (NO) by oxygen free radical (OFR) may cause endothelial dysfunction in heart failure (HF). To test this hypothesis, we examined the effect of antioxidant therapy on endothelium-dependent vasodilation of the coronary circulation in a canine model of tachycardia-induced HF. Endothelium-dependent vasodilation was less than that in controls, and OFR formation in coronary arterial and myocardial tissues was greater in HF dogs than those in controls. The immunohistochemical staining of 4-hydroxy-2-nonenal, OFR-induced lipid peroxides was detected in coronary microvessels of HF dogs. Intracoronary infusion of the cell-permeable OFR scavenger Tiron inhibited OFR formation and improved endothelium-dependent vasodilation in HF dogs but not in controls. The NO synthesis inhibitor N G-monomethyl-l-arginine (l-NMMA) diminished the beneficial effect of Tiron in HF dogs. Endothelium-independent vasodilation was similar between control and HF dogs, and no change in its response was noted by Tiron or Tiron plus l-NMMA in either group. In summary, antioxidant treatment with Tiron improved coronary vascular endothelium-dependent vasodilation by increasing NO activity in tachycardia-induced HF. Thus coronary endothelial dysfunction in HF may be, at least in part, due to increased inactivation of NO by OFR.

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