Erratum: Peripheral administration of AT1 receptor blockers and pressor responses to central angiotensin II and sodium

2001 ◽  
Vol 79 (12) ◽  
pp. 1045
Author(s):  
Jing Zhang ◽  
Frans HH Leenen
Keyword(s):  
Angiotensin Ii ◽  
At1 Receptor ◽  
Pressor Responses ◽  
Receptor Blockers ◽  
At1 Receptor Blockers

scholarly journals (Pro)renin receptor: another member of the system controlled by angiotensin II?

2011 ◽  
Vol 13 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Luciana G Pereira ◽  
Carine P Arnoni ◽  
Edgar Maquigussa ◽  
Priscila C Cristovam ◽  
Juliana Dreyfuss ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Mesangial Cells ◽  
At1 Receptor ◽  
Receptor Internalization ◽  
Prorenin Receptor ◽  
Receptor Blockers ◽  
And Function ◽  
At1 Receptor Blockers

The prorenin receptor [(P)RR] is upregulated in the diabetic kidney and has been implicated in the high glucose (HG)-induced overproduction of profibrotic molecules by mesangial cells (MCs), which is mediated by ERK1/2 phosphorylation. The regulation of (P)RR gene transcription and the mechanisms by which HG increases (P)RR gene expression are not fully understood. Because intracellular levels of angiotensin II (AngII) are increased in MCs stimulated with HG, we used this in vitro system to evaluate the possible role of AngII in (P)RR gene expression and function by comparing the effects of AT1 receptor blockers (losartan or candesartan) and (P)RR mRNA silencing (siRNA) in human MCs (HMCs) stimulated with HG. HG induced an increase in (P)RR and fibronectin expression and in ERK1/2 phosphorylation. These effects were completely reversed by (P)RR siRNA and losartan but not by candesartan (an angiotensin receptor blocker that, in contrast to losartan, blocks AT1 receptor internalization). These results suggest that (P)RR gene activity may be controlled by intracellular AngII and that HG-induced ERK1/2 phosphorylation and fibronectin overproduction are primarily induced by (P)RR activation. This relationship between AngII and (P)RR may constitute an additional pathway of MC dysfunction in response to HG stimulation.

Is it Possible to Differentiate between Angiotensin II Type 1 (AT1) Receptor Blockers in Normotensive Volunteers?

2000 ◽  
Vol 9 (sup1) ◽  
pp. 53-53
Author(s):  
M. AZIZI, ◽  
G. CHATELLIER, ◽  
L. NICOLET, ◽  
T. GUYENE, ◽  
J. HEMPENIUS, ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
At1 Receptor ◽  
Receptor Blockers ◽  
At1 Receptor Blockers

scholarly journals Facile and Efficient Syntheses of a Series of N-Benzyl and N-Biphenylmethyl Substituted Imidazole Derivatives Based on (E)-Urocanic acid, as Angiotensin II AT1 Receptor Blockers

Molecules ◽  
2013 ◽  
Vol 18 (7) ◽  
pp. 7510-7532 ◽  
Author(s):  
George Agelis ◽  
Konstantinos Kelaidonis ◽  
Amalia Resvani ◽  
Dimitra Kalavrizioti ◽  
Maria-Eleni Androutsou ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
At1 Receptor ◽  
Urocanic Acid ◽  
Imidazole Derivatives ◽  
Receptor Blockers ◽  
At1 Receptor Blockers

Role of Angiotensin II AT1 Receptor Blockers in the Treatment of Arterial Hypertension

2003 ◽  
Vol 10 (6) ◽  
pp. 401-408 ◽  
Author(s):  
Freddy Contreras ◽  
Mar??a Antonia de la Parte ◽  
Julio Cabrera ◽  
Nestor Ospino ◽  
Zafar H. Israili ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Hypertension ◽  
At1 Receptor ◽  
Receptor Blockers ◽  
At1 Receptor Blockers

scholarly journals Angiotensin II AT1 receptor blockers as treatments for inflammatory brain disorders

2012 ◽  
Vol 123 (10) ◽  
pp. 567-590 ◽  
Author(s):  
Juan M. Saavedra
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Angiotensin Ii ◽  
At1 Receptor ◽  
Brain Inflammation ◽  
Brain Disorders ◽  
Receptor Blockers ◽  
At1 Receptor Blockers

The effects of brain AngII (angiotensin II) depend on AT1 receptor (AngII type 1 receptor) stimulation and include regulation of cerebrovascular flow, autonomic and hormonal systems, stress, innate immune response and behaviour. Excessive brain AT1 receptor activity associates with hypertension and heart failure, brain ischaemia, abnormal stress responses, blood–brain barrier breakdown and inflammation. These are risk factors leading to neuronal injury, the incidence and progression of neurodegerative, mood and traumatic brain disorders, and cognitive decline. In rodents, ARBs (AT1 receptor blockers) ameliorate stress-induced disorders, anxiety and depression, protect cerebral blood flow during stroke, decrease brain inflammation and amyloid-β neurotoxicity and reduce traumatic brain injury. Direct anti-inflammatory protective effects, demonstrated in cultured microglia, cerebrovascular endothelial cells, neurons and human circulating monocytes, may result not only in AT1 receptor blockade, but also from PPARγ (peroxisome-proliferator-activated receptor γ) stimulation. Controlled clinical studies indicate that ARBs protect cognition after stroke and during aging, and cohort analyses reveal that these compounds significantly reduce the incidence and progression of Alzheimer's disease. ARBs are commonly used for the therapy of hypertension, diabetes and stroke, but have not been studied in the context of neurodegenerative, mood or traumatic brain disorders, conditions lacking effective therapy. These compounds are well-tolerated pleiotropic neuroprotective agents with additional beneficial cardiovascular and metabolic profiles, and their use in central nervous system disorders offers a novel therapeutic approach of immediate translational value. ARBs should be tested for the prevention and therapy of neurodegenerative disorders, in particular Alzheimer's disease, affective disorders, such as co-morbid cardiovascular disease and depression, and traumatic brain injury.

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