scholarly journals Role of the macula densa sodium glucose cotransporter type 1-nitric oxide synthase 1-tubuloglomerular feedback pathway in diabetic hyperfiltration.

2021 ◽  
Author(s):  
Jie Zhang ◽  
Jing Cai ◽  
Yu Cui ◽  
Shan Jiang ◽  
Jin Wei ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
Sodium Glucose Cotransporter ◽  
Nitric Oxide Synthase 1 ◽  
Oxide Synthase ◽  
Feedback Pathway

Role of macula densa neuronal nitric oxide synthase in renal diseases

2006 ◽  
Vol 39 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Akihiro Tojo ◽  
Maristela Lika Onozato ◽  
Toshiro Fujita
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Macula Densa ◽  
Renal Diseases ◽  
Oxide Synthase

scholarly journals Role of neuronal nitric oxide synthase in the macula densa

2001 ◽  
Vol 60 (5) ◽  
pp. 1676-1683 ◽  
Author(s):  
Yilin Ren ◽  
Jeffrey L. Garvin ◽  
Sadayoshi Ito ◽  
Oscar A. Carretero
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Macula Densa ◽  
Oxide Synthase

scholarly journals Suppression of Herpes Simplex Virus Type 1 (HSV-1)–induced Pneumonia in Mice by Inhibition of Inducible Nitric Oxide Synthase (iNOS, NOS2)

1997 ◽  
Vol 185 (9) ◽  
pp. 1533-1540 ◽  
Author(s):  
Heiko Adler ◽  
Janice L. Beland ◽  
Nadia C. Del-Pan ◽  
Lester Kobzik ◽  
Joanne P. Brewer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Nitric Oxide Synthase ◽  
Herpes Simplex Virus Type ◽  
Simplex Virus ◽  
Oxide Synthase ◽  
Hsv 1

Intranasal Herpes simplex virus type 1 (HSV-1) infection of mice caused pneumonia. Manifestations of the disease included: histological pneumonitis, pulmonary influx of lymphocytes, decreased pulmonary compliance, and decreased survival. Immunohistochemical staining demonstrated iNOS induction and the nitrotyrosine antigen in the lungs of infected, but not uninfected mice, suggesting that nitric oxide contributes to the development of pneumonia. To elucidate the role of nitric oxide in the pathogenesis of HSV-1 pneumonia, infected mice were treated either with the inhibitor of nitric oxide synthase activity, NG-monomethyl-l-arginine (l-NMMA), or, as a control, with PBS or d-NMMA. l-NMMA treatment decreased the histological evidence of pneumonia and reduced the bronchoalveolar lavage lymphocyte number to one-quarter of the total measured in control-treated mice. l-NMMA treatment significantly improved survival and pulmonary compliance of HSV-1–infected mice. Strikingly, the l-NMMA–mediated suppression of pneumonia occurred despite the presence of a 17-fold higher pulmonary viral titer. Taken together, these data demonstrated a previously unrecognized role of nitric oxide in HSV-1–induced pneumonia. Of note, suppression of pneumonia occurred despite higher pulmonary virus content; therefore, our data suggest that HSV-1 pneumonia is due to aspects of the inflammatory response rather than to direct viral cytopathic effects.

scholarly journals Annexin A1 inhibits macula densa Cyclooxygenase 2 and Nitric oxide Synthase 1 expression

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Alexander Paliege ◽  
Thomas Kahl ◽  
Saskia Seidel ◽  
Jürgen Schnermann ◽  
Sebastian Bachmann
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cyclooxygenase 2 ◽  
Macula Densa ◽  
Annexin A1 ◽  
Nitric Oxide Synthase 1 ◽  
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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