β-Pro7Ang III is a novel highly selective angiotensin II type 2 receptor (AT2R) agonist, which acts as a vasodepressor agent via the AT2R in conscious spontaneously hypertensive rats

2015 ◽  
Vol 129 (6) ◽  
pp. 505-513 ◽  
Author(s):  
Mark Del Borgo ◽  
Yan Wang ◽  
Sanja Bosnyak ◽  
Morimer Khan ◽  
Pia Walters ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Angiotensin Ii ◽  
Protein Binding ◽  
Binding Site ◽  
Spontaneously Hypertensive Rats ◽  
Protective Effects ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

We have synthesized a highly selective compound that is able to target a protein-binding site [called angiotensin (Ang) II type 2 receptor, AT2R] in the cardiovascular system. This research tool will enhance our ability to stimulate AT2R to produce protective effects against cardiovascular disease.

Protective effects of losartan on some type 2 diabetes mellitus-induced complications in Wistar and spontaneously hypertensive rats

2020 ◽  
Vol 35 (3) ◽  
pp. 527-538
Author(s):  
Daniela Pechlivanova ◽  
Ekaterina Krumova ◽  
Nedelina Kostadinova ◽  
Jeny Mitreva-Staleva ◽  
Petar Grozdanov ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Spontaneously Hypertensive Rats ◽  
Protective Effects ◽  
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.

scholarly journals Intrarenal Aminopeptidase N Inhibition Restores Defective Angiotensin II Type 2-Mediated Natriuresis in Spontaneously Hypertensive Rats

Hypertension ◽  
2010 ◽  
Vol 55 (2) ◽  
pp. 474-480 ◽  
Author(s):  
Shetal H. Padia ◽  
Nancy L. Howell ◽  
Brandon A. Kemp ◽  
Marie-Claude Fournie-Zaluski ◽  
Bernard P. Roques ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Aminopeptidase N ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Electroacupuncture Improved Chronic Cerebral Hypoperfusion-Induced Anxiety-Like Behavior and Memory Impairments in Spontaneously Hypertensive Rats by Downregulating the ACE/Ang II/AT1R Axis and Upregulating the ACE2/Ang-(1-7)/MasR Axis

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Peipei Feng ◽  
Zemin Wu ◽  
Hao Liu ◽  
Yafang Shen ◽  
Xu Yao ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Spontaneously Hypertensive Rats ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Memory Impairments

Electroacupuncture (EA) can effectively alleviate anxiety disorders and memory impairments caused by various neurodegenerative diseases; however, the molecular mechanisms underlying its neuroprotective effects are unclear. Previous studies have shown that the renin-angiotensin system (RAS) comprises of two axes with mutual antagonism: the classical angiotensin converting enzyme/angiotensin II/angiotensin II type 1 receptor (ACE/Ang II/AT1R) axis and the protective angiotensin converting enzyme 2/angiotensin-(1-7)/Mas receptor (ACE2/Ang-(1-7)/MasR) axis. In this study, we observed that chronic cerebral hypoperfusion (CCH) mediated anxiety-like behavior and memory impairments in spontaneously hypertensive rats (SHR) via upregulation of the hippocampal classical axis (ACE/Ang II/AT1R) and the partial hippocampal protective axis (ACE2/Ang-(1-7)). However, Ang II levels were much higher than those of Ang-(1–7), indicating that the ACE/Ang II/AT1R axis plays a dominant role in the comorbidity of CCH and hypertension. Moreover, candesartan cilexetil (Canc) and perindopril (Peril) were used as positive control drugs. We found that EA, Canc, and Peril attenuated CCH-induced anxiety-like behavior and memory impairments in SHR, potentially via downregulation of the hippocampal classical axis (ACE/Ang II/AT1R) and upregulation of the whole hippocampal protective axis (ACE2/Ang-(1-7)/MasR). These results suggest that EA therapy for CCH with hypertension may be mediated by two hippocampal RAS axes.

Protective effects of the angiotensin II type I (ATI) receptor blockade in low-renin deoxycorticosterone acetate (DOCA)-treated spontaneously hypertensive rats

2004 ◽  
Vol 106 (3) ◽  
pp. 251-259 ◽  
Author(s):  
Virginia CHAMORRO ◽  
Rosemary WANGENSTEEN ◽  
Juan SAINZ ◽  
Juan DUARTE ◽  
Francisco O'VALLE ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Urinary Excretion ◽  
Renal Injury ◽  
Spontaneously Hypertensive Rats ◽  
Ventricular Hypertrophy ◽  
Renal Cortex ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

The present study evaluates the participation of oxidative stress, tissue angiotensin II (Ang II) and endothelin (ET) in the effects of losartan on blood pressure (BP), ventricular hypertrophy and renal injury in spontaneously hypertensive rats (SHRs), and explores how these effects are modified when spontaneous hypertension is transformed in a low-renin model by the administration of deoxycorticosterone acetate (DOCA). The following groups were used: SHR-control, SHR+DOCA, SHR+losartan and SHR+DOCA+losartan. Tail systolic BP was measured once a week. After 9 weeks of treatment, direct BP and metabolic, morphological, biochemical and renal variables were measured. DOCA administration to SHRs produced an increase in BP, ventricular hypertrophy, renal weight, proteinuria, renal histopathological lesions, urinary excretion of isoprostane F2α and ET levels in the renal cortex. Losartan reduced BP, plasma malondialdehyde levels, urinary excretion of isoprostane F2α, renal Ang II and renal and urinary levels of ET in the SHR and DOCA-treated SHR groups. Losartan increased plasma nitrite/nitrate in SHRs, but not in low-renin DOCA-treated SHRs. Losartan reduced ventricular hypertrophy and ventricular Ang II in SHRs, but not in DOCA-treated SHRs. Losartan significantly decreased proteinuria and renal injury in DOCA-treated SHRs. We conclude that (i) the DOCA-induced aggravation of hypertension, ventricular hypertrophy and renal injury in SHRs is accompanied by augmented oxidative stress and increased levels of ET in the renal cortex, which could contribute to their development; and (ii) losartan reduced oxidative stress and renal Ang II and ET in SHRs and DOCA-treated SHRs, which might contribute to its antihypertensive and renoprotective effects, regardless of renin status.

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