Endothelial nitric oxide synthase is involved in calcium-induced Akt signaling in mouse skeletal muscle

Nitric Oxide ◽  
2009 ◽  
Vol 21 (3-4) ◽  
pp. 192-200 ◽  
Author(s):  
Jason A. Drenning ◽  
Vitor A. Lira ◽  
Quinlyn A. Soltow ◽  
Claire N. Canon ◽  
Lauren M. Valera ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Akt Signaling ◽  
Mouse Skeletal Muscle ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Endothelial Nitric Oxide Synthase Expression in the Sarcoplasmic Reticulum of Mouse Skeletal Muscle

2004 ◽  
Vol 37 (5) ◽  
pp. 307-311 ◽  
Author(s):  
Kyutaro Kawagishi ◽  
Fumiko Terasawa ◽  
Akinori Nakamura ◽  
Tetsuji Moriizumi ◽  
Hideho Ueda
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Mouse Skeletal Muscle ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Endothelial nitric oxide synthase (NOS) deficiency affects energy metabolism pattern in murine oxidative skeletal muscle

2002 ◽  
Vol 368 (1) ◽  
pp. 341-347 ◽  
Author(s):  
Iman MOMKEN ◽  
Dominique FORTIN ◽  
Bernard SERRURIER ◽  
Xavier BIGARD ◽  
Renée VENTURA-CLAPIER ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Nitric Oxide Synthase ◽  
Soleus Muscle ◽  
Mitochondrial Respiration ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxidative Capacity ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Oxidative capacity of muscles correlates with capillary density and with microcirculation, which in turn depend on various regulatory factors, including NO generated by endothelial nitric oxide synthase (eNOS). To determine the role of eNOS in patterns of regulation of energy metabolism in various muscles, we studied mitochondrial respiration in situ in saponin-permeabilized fibres as well as the energy metabolism enzyme profile in the cardiac, soleus (oxidative) and gastrocnemius (glycolytic) muscles isolated from mice lacking eNOS (eNOS-/-). In soleus muscle, the absence of eNOS induced a marked decrease in both basal mitochondrial respiration without ADP (-32%; P<0.05) and maximal respiration in the presence of ADP (-29%; P<0.05). Furthermore, the eNOS-/- soleus muscle showed a decrease in total creatine kinase (-29%; P<0.05), citrate synthase (-31%; P<0.01), adenylate kinase (-27%; P<0.05), glyceraldehyde-3-phosphate dehydrogenase (-43%; P<0.01) and pyruvate kinase (-26%; P<0.05) activities. The percentage of myosin heavy chains I (slow isoform) was significantly increased from 24.3±1.5% in control to 30.1±1.1% in eNOS-/- soleus muscle (P<0.05) at the expense of a slight non-significant decrease in the three other (fast) isoforms. Besides, eNOS-/- soleus showed a 28% loss of weight. Interestingly, we did not find differences in any parameters in cardiac and gastrocnemius muscles compared with respective controls. These results show that eNOS knockout has an important effect on muscle oxidative capacity as well on the activities of energy metabolism enzymes in oxidative (soleus) muscle. The absence of such effects in cardiac and glycolytic (gastrocnemius) muscle suggests a specific role for eNOS-produced NO in oxidative skeletal muscle.

scholarly journals Progesterone Attenuates Experimental Subarachnoid Hemorrhage-Induced Vasospasm by Upregulation of Endothelial Nitric Oxide Synthase via Akt Signaling Pathway

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Chia-Mao Chang ◽  
Yu-Feng Su ◽  
Chih-Zen Chang ◽  
Chia-Li Chung ◽  
Yee-Jean Tsai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Hemorrhage ◽  
Nitric Oxide Synthase ◽  
Signaling Pathway ◽  
Cerebral Vasospasm ◽  
Endothelial Nitric Oxide Synthase ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Cerebral vasospasm is the leading cause of mortality and morbidity in patients after aneurysmal subarachnoid hemorrhage (SAH). However, the mechanism and adequate treatment of vasospasm are still elusive. In the present study, we evaluate the effect and possible mechanism of progesterone on SAH-induced vasospasm in a two-hemorrhage rodent model of SAH. Progesterone (8 mg/kg) was subcutaneously injected in ovariectomized female Sprague-Dawley rats one hour after SAH induction. The degree of vasospasm was determined by averaging the cross-sectional areas of basilar artery 7 days after first SAH. Expressions of endothelial nitric oxide synthase (eNOS) and phosphorylated Akt (phospho-Akt) in basilar arteries were evaluated. Prior to perfusion fixation, there were no significant differences among the control and treated groups in physiological parameters recorded. Progesterone treatment significantly(P<0.01)attenuated SAH-induced vasospasm. The SAH-induced suppression of eNOS protein and phospho-Akt were relieved by progesterone treatment. This result further confirmed that progesterone is effective in preventing SAH-induced vasospasm. The beneficial effect of progesterone might be in part related to upregulation of expression of eNOS via Akt signaling pathway after SAH. Progesterone holds therapeutic promise in the treatment of cerebral vasospasm following SAH.

scholarly journals Endothelial nitric oxide synthase is central to skeletal muscle metabolic regulation and enzymatic signaling during exercise in vivo

2010 ◽  
Vol 298 (5) ◽  
pp. R1399-R1408 ◽  
Author(s):  
Robert S. Lee-Young ◽  
Julio E. Ayala ◽  
Charles F. Hunley ◽  
Freyja D. James ◽  
Deanna P. Bracy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Metabolic Regulation ◽  
Acid Uptake ◽  
Enos Expression ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Endothelial nitric oxide synthase (eNOS) is associated with a number of physiological functions involved in the regulation of metabolism; however, the functional role of eNOS is poorly understood. We tested the hypothesis that eNOS is critical to muscle cell signaling and fuel usage during exercise in vivo, using 16-wk-old catheterized (carotid artery and jugular vein) C57BL/6J mice with wild-type (WT), partial (+/−), or no expression (−/−) of eNOS. Quantitative reductions in eNOS expression (∼40%) elicited many of the phenotypic effects observed in enos−/− mice under fasted, sedentary conditions, with expression of oxidative phosphorylation complexes I to V and ATP levels being decreased, and total NOS activity and Ca2+/CaM kinase II Thr286 phosphorylation being increased in skeletal muscle. Despite these alterations, exercise tolerance was markedly impaired in enos−/− mice during an acute 30-min bout of exercise. An eNOS-dependent effect was observed with regard to AMP-activated protein kinase signaling and muscle perfusion. Muscle glucose and long-chain fatty acid uptake, and hepatic and skeletal muscle glycogenolysis during the exercise bout was markedly accelerated in enos−/− mice compared with enos+/− and WT mice. Correspondingly, enos−/− mice exhibited hypoglycemia during exercise. Thus, the ablation of eNOS alters a number of physiological processes that result in impaired exercise capacity in vivo. The finding that a partial reduction in eNOS expression is sufficient to induce many of the changes associated with ablation of eNOS has implications for chronic metabolic diseases, such as obesity and insulin resistance, which are associated with reduced eNOS expression.

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).

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