The role of nitric oxide signaling in pulmonary circulation of high- and low-altitude newborn sheep under basal and acute hypoxic conditions

Nitric Oxide ◽  
2019 ◽  
Vol 89 ◽  
pp. 71-80 ◽  
Author(s):  
Emilio A. Herrera ◽  
Germán Ebensperger ◽  
Ismael Hernández ◽  
Emilia M. Sanhueza ◽  
Aníbal J. Llanos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Circulation ◽  
Nitric Oxide Signaling ◽  
Hypoxic Conditions ◽  
Low Altitude

scholarly journals Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Physiology ◽  
2013 ◽  
Vol 28 (4) ◽  
pp. 216-224 ◽  
Author(s):  
John W. Calvert ◽  
David J. Lefer
Keyword(s):  
Nitric Oxide ◽  
Risk Factors ◽  
Adrenergic Receptors ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Signaling ◽  
Factors Associated ◽  
Cardioprotective Effects ◽  
Β Adrenergic Receptors

Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and β-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemia-reperfusion injury.

The role of nitric oxide signaling in renoprotective effects of hydrogen sulfide against chronic kidney disease in rats: Involvement of oxidative stress, autophagy and apoptosis

2018 ◽  
Vol 234 (7) ◽  
pp. 11411-11423 ◽  
Author(s):  
Mohammad Khabbaz Shirazi ◽  
Asaad Azarnezhad ◽  
Mohammad Foad Abazari ◽  
Mansour Poorebrahim ◽  
Pegah Ghoraeian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Hydrogen Sulfide ◽  
Kidney Disease ◽  
Nitric Oxide Signaling

Endothelial dysfunction induced by cadmium and mercury and its relationship to hypertension

2021 ◽  
Vol 17 ◽  
Author(s):  
Airton Cunha Martins ◽  
Alessanda Antunes Dos Santos ◽  
Ana Carolina B. Almeida Lopes ◽  
Anatoly V. Skalny ◽  
Michael Aschner ◽  
...  
Keyword(s):  
Public Health ◽  
Nitric Oxide ◽  
Heavy Metals ◽  
Endothelial Dysfunction ◽  
Toxic Elements ◽  
Health Concern ◽  
Public Health Concern ◽  
Important Public Health ◽  
Nitric Oxide Signaling

: Hypertension is an important public health concern that affects millions globally, leading to a large number of morbidities and fatalities. The etiology of hypertension is complex and multifactorial, and it involves environmental factors including heavy metals. Indeed, cadmium and mercury are toxic elements commonly distributed in the environment which contribute to hypertension. We aimed to assess the role of cadmium and mercury-induced endothelial dysfunction in the development of hypertension. A narrative review was carried out through database searches. In this review, we discussed the critical roles of cadmium and mercury in the etiology of hypertension and provide new insights into potential mechanisms of their effect, focusing primarily on endothelial dysfunction. Although, the mechanisms by which cadmium and mercury induce hypertension have yet to be completely elucidated, evidence for both implicates impaired nitric oxide signaling in their hypertensive etiology.

scholarly journals Erythropoietin and a nonerythropoietic peptide analog promote aortic endothelial cell repair under hypoxic conditions: role of nitric oxide

Hypoxia ◽  
2016 ◽  
Vol Volume 4 ◽  
pp. 121-133 ◽  
Author(s):  
Lamia Heikal ◽  
Pietro Ghezzi ◽  
Manuela Mengozzi ◽  
Blanka Stelmaszczuk ◽  
Martin Feelisch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Aortic Endothelial Cell ◽  
Cell Repair ◽  
Peptide Analog ◽  
Hypoxic Conditions ◽  
Aortic Endothelial

scholarly journals The role of water channel proteins and nitric oxide signaling in rice seed germination

Cell Research ◽  
2007 ◽  
Vol 17 (7) ◽  
pp. 638-649 ◽  
Author(s):  
Hong-Yan Liu ◽  
Xin Yu ◽  
Da-Yong Cui ◽  
Mei-Hao Sun ◽  
Wei-Ning Sun ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Seed Germination ◽  
Water Channel ◽  
Rice Seed ◽  
Nitric Oxide Signaling ◽  
Channel Proteins

Role of Nitric Oxide Signaling Pathways in Brain Injuries

2010 ◽  
Vol 4 (3) ◽  
pp. 250-261
Author(s):  
Maria Aurelia Zorrilla-Zubilete ◽  
Damian Gustavo Maur ◽  
Maria Laura Palumbo ◽  
Ana Maria Genaro
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Brain Injuries ◽  
Nitric Oxide Signaling

scholarly journals Shear stress stimulates nitric oxide signaling in pulmonary arterial endothelial cells via a reduction in catalase activity: role of protein kinase Cδ

2010 ◽  
Vol 298 (1) ◽  
pp. L105-L116 ◽  
Author(s):  
Sanjiv Kumar ◽  
Neetu Sud ◽  
Fabio V. Fonseca ◽  
Yali Hou ◽  
Stephen M. Black
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Catalase Activity ◽  
Serine Phosphorylation ◽  
Nitric Oxide Signaling ◽  
Enos Uncoupling ◽  
Pulmonary Arterial ◽  
Arterial Endothelial Cells

Previous studies have indicated that acute increases in shear stress can stimulate endothelial nitric oxide synthase (eNOS) activity through increased PI3 kinase/Akt signaling and phosphorylation of Ser1177. However, the mechanism by which shear stress activates this pathway has not been adequately resolved nor has the potential role of reactive oxygen species (ROS) been evaluated. Thus, the purpose of this study was to determine if shear-mediated increases in ROS play a role in stimulating Ser1177 phosphorylation and NO signaling in pulmonary arterial endothelial cells (PAEC) exposed to acute increases in shear stress. Our initial studies demonstrated that although shear stress did not increase superoxide levels in PAEC, there was an increase in H2O2 levels. The increases in H2O2 were associated with a decrease in catalase activity but not protein levels. In addition, we found that acute shear stress caused an increase in eNOS phosphorylation at Ser1177 phosphorylation and a decrease in phosphorylation at Thr495. We also found that the overexpression of catalase significantly attenuated the shear-mediated increases in H2O2, phospho-Ser1177 eNOS, and NO generation. Further investigation identified a decrease in PKCδ activity in response to shear stress, and the overexpression of PKCδ attenuated the shear-mediated decrease in Thr495 phosphorylation and the increase in NO generation, and this led to increased eNOS uncoupling. PKCδ overexpression also attenuated Ser1177 phosphorylation through a posttranslational increase in catalase activity, mediated via a serine phosphorylation event, reducing shear-mediated increases in H2O2. Together, our data indicate that shear stress decreases PKCδ activity, altering the phosphorylation pattern catalase, leading to decreased catalase activity and increased H2O2 signaling, and this in turn leads to increases in phosphorylation of eNOS at Ser1177 and NO generation.

Sign in / Sign up

Export Citation Format

Share Document