scholarly journals Effect of AT1 Receptor Blockade on Expression of Genes for Type-1 Angiotensin II(AT1) Receptor Subtypes in Spontaneously Hypertensive Rats.

1994 ◽  
Vol 17 (3) ◽  
pp. 187-192
Author(s):  
Rumi Wakamiya ◽  
Yutaka Kitami ◽  
Takafumi Okura ◽  
Katsuhiko Kohara ◽  
Kunio Hiwada
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
At1 Receptor ◽  
Receptor Subtypes ◽  
Receptor Blockade ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Expression Of Genes

scholarly journals Angiotensin II Type 1 Receptor Blocker Reduces Monocyte Adhesion to Endothelial Cells in Spontaneously Hypertensive Rats

2007 ◽  
Vol 54 (4) ◽  
pp. 605-612 ◽  
Author(s):  
Fuki IKEDA ◽  
Kosuke AZUMA ◽  
Takeshi OGIHARA ◽  
Yukiko TOYOFUKU ◽  
Aiko OTSUKA ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Receptor Blocker ◽  
Monocyte Adhesion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Angiotensin II AT1 Receptor Blockade Abolishes Brain Microvascular Inflammation and Heat Shock Protein Responses in Hypertensive Rats

2005 ◽  
Vol 25 (7) ◽  
pp. 878-886 ◽  
Author(s):  
Jin Zhou ◽  
Hiromichi Ando ◽  
Miroslava Macova ◽  
Jingtao Dou ◽  
Juan M Saavedra
Keyword(s):  
Angiotensin Ii ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Receptor Antagonist ◽  
Spontaneously Hypertensive Rats ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Cerebral Microvessels ◽  
Spontaneously Hypertensive

Endothelial dysfunction and inflammation enhance vulnerability to hypertensive brain damage. To explore the participation of Angiotensin II (Ang II) in the mechanism of vulnerability to cerebral ischemia during hypertension, we examined the expression of inflammatory factors and the heat shock protein (HSP) response in cerebral microvessels from spontaneously hypertensive rats and their normotensive controls, Wistar Kyoto rats. We treated animals with vehicle or the Ang II AT1 receptor antagonist candesartan, 0.3 mg/kg/day, via subcutaneously implanted osmotic minipumps for 4 weeks. Spontaneously hypertensive rats expressed higher Angiotensin II AT1 receptor protein and mRNA than normotensive controls. Candesartan decreased the macrophage infiltration and reversed the enhanced tumor necrosis factor-α and interleukin-1β mRNA and nuclear factor-κB in microvessels in hypertensive rats. The transcription of many HSP family genes, including HSP60, HSP70 and HSP90, and heat shock factor-1 was higher in hypertensive rats and was downregulated by AT1 receptor blockade. Our results suggest a proinflammatory action of Ang II through AT1 receptor stimulation in cerebral microvessels during hypertension, and very potent antiinflammatory effects of the Ang II AT1 receptor antagonist. These compounds might be considered as potential therapeutic agents against ischemic and inflammatory diseases of the brain.

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