Cellular Mechanisms of Inflammatory Mediators Acting on Vagal Sensory Nerve Excitability

1995 ◽  
Vol 8 (4-5) ◽  
pp. 173-179 ◽  
Author(s):  
Daniel Weinreich
2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Hui Sun ◽  
Mayur Patil ◽  
Fei Ru ◽  
Sonya Meeker ◽  
Bradley J. Undem

2008 ◽  
Vol 119 (3) ◽  
pp. e22
Author(s):  
Susanna B. Park ◽  
Cindy S.-Y. Lin ◽  
Arun V. Krishnan ◽  
Michael Friedlander ◽  
David Goldstein ◽  
...  

2014 ◽  
Vol 125 ◽  
pp. S267
Author(s):  
Y. Osaki ◽  
H. Nodera ◽  
Y. Shimatani ◽  
B. Chimeglkham ◽  
R. Kaji

2008 ◽  
Vol 15 (3) ◽  
pp. 362
Author(s):  
Cindy Shin-Yi Lin ◽  
Arun Krishnan ◽  
David Goldstein ◽  
Michael Friedlander ◽  
Matthew Kiernan

Author(s):  
Hao-Wen Teng ◽  
Jowy Tani ◽  
Tsui-San Chang ◽  
Hung-Ju Chen ◽  
Yi-Chen Lin ◽  
...  

2007 ◽  
Vol 43 ◽  
pp. 105-120 ◽  
Author(s):  
Michael L. Paffett ◽  
Benjimen R. Walker

Several molecular and cellular adaptive mechanisms to hypoxia exist within the vasculature. Many of these processes involve oxygen sensing which is transduced into mediators of vasoconstriction in the pulmonary circulation and vasodilation in the systemic circulation. A variety of oxygen-responsive pathways, such as HIF (hypoxia-inducible factor)-1 and HOs (haem oxygenases), contribute to the overall adaptive process during hypoxia and are currently an area of intense research. Generation of ROS (reactive oxygen species) may also differentially regulate vascular tone in these circulations. Potential candidates underlying the divergent responses between the systemic and pulmonary circulations may include Nox (NADPH oxidase)-derived ROS and mitochondrial-derived ROS. In addition to alterations in ROS production governing vascular tone in the hypoxic setting, other vascular adaptations are likely to be involved. HPV (hypoxic pulmonary vasoconstriction) and CH (chronic hypoxia)-induced alterations in cellular proliferation, ionic conductances and changes in the contractile apparatus sensitivity to calcium, all occur as adaptive processes within the vasculature.


2020 ◽  
Vol 134 (12) ◽  
pp. 1403-1432 ◽  
Author(s):  
Manal Muin Fardoun ◽  
Dina Maaliki ◽  
Nabil Halabi ◽  
Rabah Iratni ◽  
Alessandra Bitto ◽  
...  

Abstract Flavonoids are polyphenolic compounds naturally occurring in fruits and vegetables, in addition to beverages such as tea and coffee. Flavonoids are emerging as potent therapeutic agents for cardiovascular as well as metabolic diseases. Several studies corroborated an inverse relationship between flavonoid consumption and cardiovascular disease (CVD) or adipose tissue inflammation (ATI). Flavonoids exert their anti-atherogenic effects by increasing nitric oxide (NO), reducing reactive oxygen species (ROS), and decreasing pro-inflammatory cytokines. In addition, flavonoids alleviate ATI by decreasing triglyceride and cholesterol levels, as well as by attenuating inflammatory mediators. Furthermore, flavonoids inhibit synthesis of fatty acids and promote their oxidation. In this review, we discuss the effect of the main classes of flavonoids, namely flavones, flavonols, flavanols, flavanones, anthocyanins, and isoflavones, on atherosclerosis and ATI. In addition, we dissect the underlying molecular and cellular mechanisms of action for these flavonoids. We conclude by supporting the potential benefit for flavonoids in the management or treatment of CVD; yet, we call for more robust clinical studies for safety and pharmacokinetic values.


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