Nitric oxide positively regulates Ag (I)-induced Ca2+ influx and mast cell activation: role of a nitric oxide synthase-independent pathway

2009 ◽  
Vol 86 (6) ◽  
pp. 1365-1375 ◽  
Author(s):  
Toshio Inoue ◽  
Yoshihiro Suzuki ◽  
Tetsuro Yoshimaru ◽  
Chisei Ra
Keyword(s):  
Nitric Oxide ◽  
Mast Cell ◽  
Nitric Oxide Synthase ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Oxide Synthase

Vasculoprotective Role of Inducible Nitric Oxide Synthase at Inflammatory Coronary Lesions Induced by Chronic Treatment With Interleukin-1β in Pigs in Vivo

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3104-3111 ◽  
Author(s):  
Yoshihiro Fukumoto ◽  
Hiroaki Shimokawa ◽  
Toshiyuki Kozai ◽  
Toshiaki Kadokami ◽  
Kouichi Kuwata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Chronic Treatment ◽  
Interleukin 1Β ◽  
Coronary Lesions ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Neuronal nitric oxide synthase and systemic vasodilation in rats with cirrhosis

2000 ◽  
Vol 279 (6) ◽  
pp. F1110-F1115 ◽  
Author(s):  
Lieming Xu ◽  
Ethan P. Carter ◽  
Mamiko Ohara ◽  
Pierre-Yves Martin ◽  
Boris Rogachev ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Cirrhosis ◽  
Nitric Oxide Synthase ◽  
Control Treatment ◽  
Sodium Balance ◽  
Hyperdynamic Circulation ◽  
Molecular Approaches ◽  
Advanced Liver Cirrhosis ◽  
Oxide Synthase

Cirrhosis is typically associated with a hyperdynamic circulation consisting of low blood pressure, low systemic vascular resistance (SVR), and high cardiac output. We have recently reported that nonspecific inhibition of nitric oxide synthase (NOS) with nitro-l-arginine methyl ester reverses the hyperdynamic circulation in rats with advanced liver cirrhosis induced by carbon tetrachloride (CCl4). Although an important role for endothelial NOS (eNOS) is documented in cirrhosis, the role of neuronal NOS (nNOS) has not been investigated. The present study was carried out to specifically investigate the role of nNOS during liver cirrhosis. Specifically, physiological, biochemical, and molecular approaches were employed to evaluate the contribution of nNOS to the cirrhosis-related hyperdynamic circulation in CCl4-induced cirrhotic rats with ascites. Cirrhotic animals had a significant increase in water and sodium retention. In the aorta from cirrhotic animals, both nNOS protein expression and cGMP concentration were significantly elevated compared with control. Treatment of cirrhotic rats for 7 days with the specific nNOS inhibitor 7-nitroindazole (7-NI) normalized the low SVR and mean arterial pressure, elevated cardiac index, and reversed the positive sodium balance. Increased plasma arginine vasopressin concentrations in the cirrhotic animals were also repressed with 7-NI in association with diminished water retention. The circulatory changes were associated with a reduction in aortic nNOS expression and cGMP. However, 7-NI treatment did not restore renal function in cirrhotic rats (creatinine clearance: 0.76 ± 0.03 ml · min−1· 100 g body wt−1in cirrhotic rats vs. 0.79 ± 0.05 ml · min−1· 100 g body wt−1in cirrhotic rats+7-NI; P NS.). Taken together, these results indicate that nNOS-derived NO contributes to the development of the hyperdynamic circulation and fluid retention in cirrhosis.

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