Nitric oxide synthase inhibition speeds oxygen uptake kinetics in horses during moderate domain running

2002 ◽  
Vol 132 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Casey A Kindig ◽  
Paul McDonough ◽  
Howard H Erickson ◽  
David C Poole
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxygen Uptake ◽  
Oxygen Uptake Kinetics ◽  
Uptake Kinetics ◽  
Oxide Synthase

scholarly journals Effects of nitric oxide synthase inhibition byl-NAME on oxygen uptake kinetics in isolated canine musclein situ

2005 ◽  
Vol 568 (3) ◽  
pp. 1021-1033 ◽  
Author(s):  
Bruno Grassi ◽  
Michael C. Hogan ◽  
Kevin M. Kelley ◽  
Richard A. Howlett ◽  
L. Bruce Gladden
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxygen Uptake ◽  
Oxygen Uptake Kinetics ◽  
Uptake Kinetics ◽  
Oxide Synthase

Mitochondrial Nitric Oxide Synthase: A Masterpiece of Metabolic Adaptation, Cell Growth, Transformation, and Death

2009 ◽  
Vol 234 (9) ◽  
pp. 1020-1028 ◽  
Author(s):  
Paola V. Finocchietto ◽  
Maria C. Franco ◽  
Silvia Holod ◽  
Analia S. Gonzalez ◽  
Daniela P. Converso ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxygen Uptake ◽  
Reduction Reaction ◽  
Metabolic Adaptation ◽  
Oxidation Reduction ◽  
Mitochondrial Nitric Oxide Synthase ◽  
Dependent Cell ◽  
Cell Arrest ◽  
Oxide Synthase

Mitochondria are specialized organelles that control energy metabolism and also activate a multiplicity of pathways that modulate cell proliferation and mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO) regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the production of superoxide anion from the mitochondrial electron transfer chain. In this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to oxidation-reduction reaction (redox)–dependent cell signaling. Modulation of translocation and activation of neuronal nitric oxide synthase (mtNOS activity) under different physiologic or pathologic conditions represents an adaptive response properly modulated to adjust mitochondria to different cell challenges.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Nitric oxide synthase and cellac disease

2001 ◽  
Vol 120 (5) ◽  
pp. A684-A684
Author(s):  
I DANIELS ◽  
I MURRAY ◽  
W GODDARD ◽  
R LONG
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxide Synthase
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