Angiotensin II Type 1 Receptor-Dependent Nuclear Factor-κB Activation-Mediated Proinflammatory Actions in a Rat Model of Obstructive Acute Pancreatitis

2007 ◽  
Vol 323 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Yuk Cheung Chan ◽  
Po Sing Leung
Keyword(s):  
Acute Pancreatitis ◽  
Angiotensin Ii ◽  
Rat Model ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

Suppression of Diabetes-Induced Retinal Inflammation by Blocking the Angiotensin II Type 1 Receptor or Its Downstream Nuclear Factor-κB Pathway

2007 ◽  
Vol 48 (9) ◽  
pp. 4342 ◽  
Author(s):  
Norihiro Nagai ◽  
Kanako Izumi-Nagai ◽  
Yuichi Oike ◽  
Takashi Koto ◽  
Shingo Satofuka ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Retinal Inflammation

Angiotensin II Type 1 receptor blockade protects endothelium-derived hyperpolarising factor-mediated relaxation in a rat model of monoarthritis

Life Sciences ◽  
2013 ◽  
Vol 92 (23) ◽  
pp. 1131-1137 ◽  
Author(s):  
Andrew MacKenzie ◽  
Lynette Dunning ◽  
William R. Ferrell ◽  
John C. Lockhart
Keyword(s):  
Angiotensin Ii ◽  
Rat Model ◽  
Receptor Blockade

scholarly journals Endoplasmic reticulum and oxidant stress mediate nuclear factor-κB activation in the subfornical organ during angiotensin II hypertension

2015 ◽  
Vol 308 (10) ◽  
pp. C803-C812 ◽  
Author(s):  
Colin N. Young ◽  
Anfei Li ◽  
Frederick N. Dong ◽  
Julie A. Horwath ◽  
Catharine G. Clark ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endoplasmic Reticulum ◽  
Transcription Factor ◽  
Angiotensin Ii ◽  
Er Stress ◽  
Bioluminescence Imaging ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Ang Ii ◽  
Arterial Blood

Endoplasmic reticulum (ER) stress and reactive oxygen species (ROS) generation in the brain circumventricular subfornical organ (SFO) mediate the central hypertensive actions of Angiotensin II (ANG II). However, the downstream signaling events remain unclear. Here we tested the hypothesis that angiotensin type 1a receptors (AT1aR), ER stress, and ROS induce activation of the transcription factor nuclear factor-κB (NF-κB) during ANG II-dependent hypertension. To spatiotemporally track NF-κB activity in the SFO throughout the development of ANG II-dependent hypertension, we used SFO-targeted adenoviral delivery and longitudinal bioluminescence imaging in mice. During low-dose infusion of ANG II, bioluminescence imaging revealed a prehypertensive surge in NF-κB activity in the SFO at a time point prior to a significant rise in arterial blood pressure. SFO-targeted ablation of AT1aR, inhibition of ER stress, or adenoviral scavenging of ROS in the SFO prevented the ANG II-induced increase in SFO NF-κB. These findings highlight the utility of bioluminescence imaging to longitudinally track transcription factor activation during the development of ANG II-dependent hypertension and reveal an AT1aR-, ER stress-, and ROS-dependent prehypertensive surge in NF-κB activity in the SFO. Furthermore, the increase in NF-κB activity before a rise in arterial blood pressure suggests a causal role for SFO NF-κB in the development of ANG II-dependent hypertension.

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