Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity

2012 ◽  
Vol 5 (2) ◽  
pp. 566-574
Author(s):  
Mojca Stojiljkovic ◽  
Zorica Zakula ◽  
Goran Koricanac ◽  
Tijana Milosavljevic ◽  
Snezana Tepavcevic ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Type I Diabetes ◽  
Arginase Activity ◽  
Type I ◽  
Acute Type ◽  
Oxide Synthase

The ocular hemodynamic response to nitric oxide synthase inhibition is unaltered in patients with early type I diabetes

2003 ◽  
Vol 241 (8) ◽  
pp. 619-624 ◽  
Author(s):  
Guido T. Dorner ◽  
Gerhard Garhöfer ◽  
Nicole Selenko ◽  
Peter Fasching ◽  
Michaela Bayerle-Eder ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Type I Diabetes ◽  
Hemodynamic Response ◽  
Type I ◽  
Early Type ◽  
Oxide Synthase

Nitric oxide synthase type I and type III gene expression are developmentally regulated in rat lung

1994 ◽  
Vol 266 (6) ◽  
pp. L635-L641 ◽  
Author(s):  
A. J. North ◽  
R. A. Star ◽  
T. S. Brannon ◽  
K. Ujiie ◽  
L. B. Wells ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Fetal Lung ◽  
Mrna Abundance ◽  
Type I ◽  
Fetal Life ◽  
Rat Lung ◽  
Developmentally Regulated ◽  
Oxide Synthase

The successful transition from fetal to neonatal life involves a marked decline in pulmonary vascular resistance which is modulated in part by endothelium-derived nitric oxide. To define the molecular processes which prepare the pulmonary circulation for nitric oxide mediation of vasodilatation at the time of birth, we determined the ontogeny of endothelial nitric oxide synthase (NOS-III) gene expression in lungs from fetal and newborn rats. Maturational changes in lung neuronal NOS (NOS-I) expression were also investigated; the latter isoform has been localized to rat bronchiolar epithelium. NOS proteins were examined by immunoblot analysis, and mRNA abundance was assessed in reverse transcription-polymerase chain reaction assays. Both NOS-III and NOS-I protein were detectable in 16-day fetal lung, they increased 3.8- and 3.1-fold, respectively, to maximal levels at 20 days of gestation (term = 22 day), and they fell postnatally (1-5 days). In parallel with the findings for NOS-III protein, NOS-III mRNA increased from 16 to 20 days gestation and fell after birth. In contrast, NOS-I mRNA abundance declined during late fetal life and rose postnatally. These findings were confirmed by Northern analyses. Thus NOS-III and NOS-I gene expression are developmentally regulated in rat lung, with maximal NOS-III and NOS-I protein present near term. The regulation of pulmonary NOS-III may primarily involve alterations in transcription or mRNA stability, whereas NOS-I expression in the maturing lung may also be mediated by additional posttranscriptional processes.

scholarly journals Mechanisms of Reduced Striatal NMDA Excitotoxicity in Type I Nitric Oxide Synthase Knock-Out Mice

1997 ◽  
Vol 17 (18) ◽  
pp. 6908-6917 ◽  
Author(s):  
Cenk Ayata ◽  
Gamze Ayata ◽  
Hideaki Hara ◽  
Russel T. Matthews ◽  
M. Flint Beal ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Type I ◽  
Knock Out ◽  
Knock Out Mice ◽  
Oxide Synthase

scholarly journals Phenolic Compounds as Arginase Inhibitors: New Insights Regarding Endothelial Dysfunction Treatment

Planta Medica ◽  
2018 ◽  
Vol 84 (05) ◽  
pp. 277-295 ◽  
Author(s):  
Bruno Minozzo ◽  
Daniel Fernandes ◽  
Flávio Beltrame
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
Vascular Function ◽  
Negative Impact ◽  
Therapeutic Option ◽  
Arginase Activity ◽  
Pubmed Database ◽  
Oxide Synthase ◽  
Arginase Inhibitors

AbstractEndothelial dysfunction is characterised by the low bioavailability of nitric oxide with a relevant negative impact on the nitric oxide/cGMP pathway. The loss of nitric oxide/cGMP signaling may be caused by an increased arginase activity. Plant-derived substances, especially polyphenols, are compounds that have the potential to inhibit arginase activity and they may represent an attractive therapeutic option to combat clinical outcomes related to endothelial dysfunction. An extensive review was carried out using all available data published in English in the Pubmed database, and without restriction regarding the year of publication. Despite the increased number of new substances that have been tested as arginase inhibitors, it is rare to find a compound that satisfies all the toxicological criteria to be used in the development of a new drug. On the other hand, recent data have shown that substances from plants have great potential to be applied as arginase inhibitors, most of which are polyphenols. Of the relevant mechanisms in this process, the inhibition of arginase by natural products seems to act against endothelial dysfunction by reestablishing the vascular function and elevating nitric oxide levels (by increasing the amounts of substrate (L-arginine, and endothelial nitric oxide synthase activation and stabilisation) as well as decreasing the generation of reactive species (formed by uncoupledendothelial nitric oxide synthase). This review summarises several topics regarding arginase inhibition by natural substances as well as indicating this pathway as an emergent strategy to elevate nitric oxide levels in disorders involving endothelial dysfunction. In addition, some aspects regarding structural activity and future perspectives are discussed.

Induction and variants of neuronal nitric oxide synthase type I during synaptogenesis

1995 ◽  
Vol 9 (9) ◽  
pp. 799-806 ◽  
Author(s):  
Patricia Ogilvie ◽  
Karl Schilling ◽  
Melvin L. Bllllngslev ◽  
Harald H. H. W. Schmidt
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Type I ◽  
Oxide Synthase
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