scholarly journals Constitutively Active Mutant N111G of Angiotensin II Type 1 (AT1) Receptor Induces Homologous Internalization Through Mediation of AT1-Receptor Antagonist

2009 ◽  
Vol 111 (3) ◽  
pp. 227-234 ◽  
Author(s):  
Mohiuddin Ahmed Bhuiyan ◽  
Murad Hossain ◽  
Shin-ichiro Miura ◽  
Takashi Nakamura ◽  
Masanobu Ozaki ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
At1 Receptor ◽  
Constitutively Active

scholarly journals Effects of YM358, an Angiotensin II Type 1(AT1) Receptor Antagonist, and Enalapril on Blood Pressure and Vasoconstriction in Two Renal Hypertension Models.

2000 ◽  
Vol 23 (2) ◽  
pp. 174-181 ◽  
Author(s):  
Tomoko TOKIOKA ◽  
Masayuki SHIBASAKI ◽  
Akira FUJIMORI ◽  
Yasuko MATSUDA-SATOH ◽  
Wataru UCHIDA ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Renal Hypertension ◽  
At1 Receptor

Angiotensin II type 1 receptor blockade restores angiotensin-(1–7)-induced coronary vasodilation in hypertrophic rat hearts

2013 ◽  
Vol 125 (9) ◽  
pp. 449-459 ◽  
Author(s):  
Álvaro P. S. Souza ◽  
Deny B. S. Sobrinho ◽  
Jônathas F. Q. Almeida ◽  
Gisele M. M. Alves ◽  
Larissa M. Macedo ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
At1 Receptor ◽  
At2 Receptor ◽  
Receptor Blockade ◽  
Coronary Vasodilation ◽  
Mas Receptor ◽  
Rat Hearts ◽  
Pre Treatment

The aim of the present study was to investigate the coronary effects of Ang-(1–7) [angiotensin-(1–7)] in hypertrophic rat hearts. Heart hypertrophy was induced by abdominal aorta CoA (coarctation). Ang-(1–7) and AVE 0991, a non-peptide Mas-receptor agonist, at picomolar concentration, induced a significant vasodilation in hearts from sham-operated rats. These effects were blocked by the Mas receptor antagonist A-779. Pre-treatment with L-NAME (NG-nitro-L-arginine methyl ester) or ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinozalin-1-one) [NOS (NO synthase) and soluble guanylate cyclase inhibitors respectively] also abolished the effect of Ang-(1–7) in control hearts. The coronary vasodilation produced by Ang-(1–7) and AVE 0991 was completely blunted in hypertrophic hearts. Chronic oral administration of losartan in CoA rats restored the coronary vasodilation effect of Ang-(1–7). This effect was blocked by A-779 and AT2 receptor (angiotensin II type 2 receptor) antagonist PD123319. Acute pre-incubation with losartan also restored the Ang-(1–7)-induced, but not BK (bradykinin)-induced, coronary vasodilation in hypertrophic hearts. This effect was inhibited by A-779, PD123319 and L-NAME. Chronic treatment with losartan did not change the protein expression of Mas and AT2 receptor and ACE (angiotensin-converting enzyme) and ACE2 in coronary arteries from CoA rats, but induced a slight increase in AT2 receptor in aorta of these animals. Ang-(1–7)-induced relaxation in aortas from sham-operated rats was absent in aortas from CoA rats. In vitro pre-treatment with losartan restored the Ang-(1–7)-induced relaxation in aortic rings of CoA rats, which was blocked by the Mas antagonist A-779 and L-NAME. These data demonstrate that Mas is strongly involved in coronary vasodilation and that AT1 receptor (angiotensin II type 1 receptor) blockade potentiates the vasodilatory effects of Ang-(1–7) in the coronary beds of pressure-overloaded rat hearts through NO-related AT2- and Mas-receptor-dependent mechanisms. These data suggest the association of Ang-(1–7) and AT1 receptor antagonists as a potential therapeutic avenue for coronary artery diseases.

Involvement of Runx3 in the basal transcriptional activation of the mouse angiotensin II type 1 receptor-associated protein gene

2011 ◽  
Vol 43 (14) ◽  
pp. 884-894 ◽  
Author(s):  
Miyuki Matsuda ◽  
Kouichi Tamura ◽  
Hiromichi Wakui ◽  
Toru Dejima ◽  
Akinobu Maeda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Transcriptional Activation ◽  
At1 Receptor ◽  
Distal Convoluted Tubule ◽  
Luciferase Assay ◽  
Serum Starvation ◽  
Receptor Associated Protein ◽  
Tubule Cells

We previously cloned a molecule that interacts with angiotensin II type 1 (AT1) receptor to exert an inhibitory function on AT1 receptor signaling that we named ATRAP/ Agtrap (for AT1 receptor-associated protein). In the present study we examined the regulation of basal ATRAP gene expression using renal distal convoluted tubule cells. We found that serum starvation upregulated basal expression of ATRAP gene, a response that required de novo mRNA and protein synthesis. Luciferase assay revealed that the proximal promoter region directs transcription and that a putative binding site of runt-related transcription factors (RBE) is important for transcriptional activation. The results of RBE-decoy transfection and endogenous knockdown by small interference RNA showed that the runt-related transcription factor Runx3 is involved in ATRAP gene expression. Chromatin immunoprecipitation assay also supported the binding of Runx3 to the ATRAP promoter in renal distal convoluted tubule cells. Immunohistochemistry demonstrated the expression of Runx3 and ATRAP proteins in the distal convoluted and connecting tubules of the kidney in consecutive sections. Furthermore, the Runx3 immunostaining was decreased together with a concomitant suppression of ATRAP expression in the affected kidney after 7 days of unilateral ureteral obstruction. These findings indicate that Runx3 plays a role in ATRAP gene expression in renal distal tubular cells both in vitro and in vivo.

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