Calcium/calmodulin-dependent nitric oxide synthase type I: a biopteroflavoprotein with calcium/calmodulin-independent diaphorase and reductase activities

Biochemistry ◽  
1992 ◽  
Vol 31 (12) ◽  
pp. 3243-3249 ◽  
Author(s):  
Harald H. H. W. Schmidt ◽  
R. M. Smith ◽  
M. Nakane ◽  
Ferid Murad
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Type I ◽  
Calcium Calmodulin Dependent ◽  
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

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

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

Type I nitric oxide synthase in the human lung is predominantly expressed in capillary endothelial cells

2002 ◽  
Vol 129 (3) ◽  
pp. 367-374 ◽  
Author(s):  
Hardi Lührs ◽  
Thomas Papadopoulos ◽  
Harald H.H.W Schmidt ◽  
Thomas Menzel
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Nitric Oxide Synthase ◽  
Human Lung ◽  
Type I ◽  
Capillary Endothelial Cells ◽  
Oxide Synthase
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