Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: A genetic approach using knockout mice

2006 ◽  
Vol 23 (1) ◽  
pp. 219-227 ◽  
Author(s):  
Anne Pereira de Vasconcelos ◽  
Véronique Riban ◽  
Claude Wasterlain ◽  
Astrid Nehlig
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Knockout Mice ◽  
Endothelial Nitric Oxide Synthase ◽  
Genetic Approach ◽  
Flow Changes ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Rapid nontranscriptional activation of endothelial nitric oxide synthase mediates increased cerebral blood flow and stroke protection by corticosteroids

2003 ◽  
Vol 111 (5) ◽  
pp. 759-759
Author(s):  
Florian P. Limbourg ◽  
Zhihong Huang ◽  
Jean-Christophe Plumier ◽  
Tommaso Simoncini ◽  
Masayuki Fujioka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals 106 Role of neuronal vs endothelial nitric oxide synthase in the coronary blood flow response to pacing

Heart ◽  
2012 ◽  
Vol 98 (Suppl 1) ◽  
pp. A60.2-A61
Author(s):  
H Shabeeh ◽  
N Melikian ◽  
R Dworakowski ◽  
B Casadei ◽  
P Chowienczyk ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Coronary Blood Flow ◽  
Endothelial Nitric Oxide Synthase ◽  
Blood Flow Response ◽  
Flow Response ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Rapid nontranscriptional activation of endothelial nitric oxide synthase mediates increased cerebral blood flow and stroke protection by corticosteroids

2002 ◽  
Vol 110 (11) ◽  
pp. 1729-1738 ◽  
Author(s):  
Florian P. Limbourg ◽  
Zhihong Huang ◽  
Jean-Christophe Plumier ◽  
Tommaso Simoncini ◽  
Masayuki Fujioka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Erection Capability Is Potentiated by Long-Term Sildenafil Treatment: Role of Blood Flow-Induced Endothelial Nitric-Oxide Synthase Phosphorylation

2005 ◽  
Vol 68 (1) ◽  
pp. 226-232 ◽  
Author(s):  
Biljana Musicki ◽  
Hunter C. Champion ◽  
Robyn E. Becker ◽  
Tongyun Liu ◽  
Melissa F. Kramer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Endothelial nitric oxide synthase-deficient mice exhibit increased susceptibility to endotoxin-induced acute renal failure

2004 ◽  
Vol 287 (5) ◽  
pp. F1044-F1048 ◽  
Author(s):  
Wei Wang ◽  
Amit Mitra ◽  
Brian Poole ◽  
Sandor Falk ◽  
M. Scott Lucia ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Knockout Mice ◽  
Endothelial Nitric Oxide Synthase ◽  
Wild Type ◽  
In The Wild ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Acute renal failure (ARF) in septic patients drastically increases the mortality to 50–80%. Nitric oxide (NO) has been shown to be increased in sepsis. Endothelial nitric oxide synthase (eNOS) is one of the major regulators of arterial blood pressure and regional blood flow; however, its in vivo role in septic ARF is still unclear. We hypothesized that eNOS affords a protective effect against the renal vasoconstriction during endotoxemia. Because there are no specific inhibitors for eNOS, the study was therefore undertaken in eNOS knockout mice. There was no significant difference in baseline glomerular filtration rate (GFR) between the wild-type mice and the eNOS knockout mice (140 ± 10 vs. 157 ± 18 μl/min, n = 9, P = not significant). However, renal blood flow (RBF) was significantly decreased in eNOS knockout mice compared with the wild-type controls (0.62 ± 0.05 ml/min, n = 6 vs. 0.98 ± 0.13 ml/min, n = 8, P < 0.05). Mean arterial pressure (MAP) was significantly higher in eNOS knockout mice than the wild-type controls (109 ± 5 vs. 80 ± 1 mmHg, n = 10, P < 0.01). Thus renal vascular resistance (RVR) was much higher in eNOS knockout mice than in the wild-type mice (176 ± 2, n = 6 vs. 82 ± 1 mmHg·ml−1·min−1, n = 8, P < 0.01). When 1.0 mg/kg LPS was injected, there was no change in MAP in either the wild-type (84 ± 3 mmHg, n = 10) or the eNOS knockout mice (105 ± 5 mmHg, n = 10). Although GFR (154 ± 22 μl/min, n = 8) and RBF (1.19 ± 0.05 ml/min, n = 9) remained unchanged with the 1.0-mg/kg dose of LPS in the wild-type mice, GFR (83 ± 18 vs. 140 ± 10 μl/min, n = 6, P < 0.01) and RBF (0.36 ± 0.04 vs. 0.62 ± 0.05 ml/min, n = 6, P < 0.01) decreased significantly in the eNOS knockout mice. Fractional excretion of sodium increased significantly in eNOS knockout mice during endotoxemia (3.61 ± 0.78, n = 7 vs. 0.95 ± 0.14, n = 6, P < 0.01), whereas it remained unchanged in the wild-type mice (0.59 ± 0.16, n = 9 vs. 0.42 ± 0.05, n = 6, P = not significant). In summary, eNOS knockout mice have increased RVR and are more susceptible to endotoxemic ARF than wild-type mice despite higher MAP.

scholarly journals Dietary nitrate increases gastric mucosal blood flow and mucosal defense

2007 ◽  
Vol 292 (3) ◽  
pp. G718-G724 ◽  
Author(s):  
Joel Petersson ◽  
Mia Phillipson ◽  
Emmelie Å. Jansson ◽  
Andreas Patzak ◽  
Jon O. Lundberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Endothelial Nitric Oxide Synthase ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Dietary Nitrate ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Deficient Mice

Salivary nitrate from dietary or endogenous sources is reduced to nitrite by oral bacteria. In the acidic stomach, nitrite is further reduced to bioactive nitrogen oxides, including nitric oxide (NO). In this study, we investigated the gastroprotective role of nitrate intake and of luminally applied nitrite against provocation with diclofenac and taurocholate. Mucosal permeability (51Cr-EDTA clearance) and gastric mucosal blood flow (laser-Doppler flowmetry) were measured in anesthetized rats, either pretreated with nitrate in the drinking water or given acidified nitrite luminally. Diclofenac was given intravenously and taurocholate luminally to challenge the gastric mucosa. Luminal NO content and nitrite content in the gastric mucus were determined by chemiluminescence. The effect of luminal administration of acidified nitrite on the mucosal blood flow was also investigated in endothelial nitric oxide synthase-deficient mice. Rats pretreated with nitrate or given nitrite luminally had higher gastric mucosal blood flow than controls. Permeability increased more during the provocation in the controls than in the nitrate- and nitrite-treated animals. Dietary nitrate increased luminal NO levels 50 times compared with controls. Nitrate intake also resulted in nitrite accumulation in the loosely adherent mucous layer; after removal of this mucous layer, blood flow was reduced. Nitrite administrated luminally in endothelial nitric oxide synthase-deficient mice increased mucosal blood flow. We conclude that dietary nitrate and direct luminal application of acidified nitrite decrease diclofenac- and taurocholate-induced mucosal damage. The gastroprotective effect likely involves a higher mucosal blood flow caused by nonenzymatic NO production. These data suggest an important physiological role of nitrate in the diet.

Sign in / Sign up

Export Citation Format

Share Document