Role of angiotensin II and angiotensin type-1 receptor in scorpion venom-induced cardiac and aortic tissue inflammation

P25 We investigated effects of subpressor dose of angiotensin II (ANG II) on the vasodilating effect of Glyceryl trinitrate (GTN)in 9 normotensive healthy males. GTN at 100, 250, 1000 ng/min was intra-arterially infused with ANG II at 1, 5 pmol/min or placebo (protocol 1) with noradrenaline (NA) at 50 pmol/min or placebo (protocol 2). Effect of intra-arterial infusion of vitamin C at 25 mg/min on the interaction between GTN and ANG II was also tested (protocol 3).Protocol 1 was repeated after single oral dose of angiotensin type 1 receptor blocker, Candesartan (8mg) or matched placebo (protocol 4). Forearm blood flow (FBF) was measured by strain gauge plethymograph. ANG II significantly and dose-dependently attenuated the vasodilating effect of GTN (means±S.D. of % changes of FBF: 28±8, 79±22, 208±28 % at 100, 250, 1000 pmol/min of GTN with placebo, 8±6, 47±13, 173±31 with ANG II 1 pmol/min, 2±10, 39±13, 132±23 with ANG II 5 pmol/min. P=0.0057 vs placebo by ANOVA).NA did not affect the vasodilating effect of GTN. Co-infusion of vitamin C (25 mg/min)completely abolished the the interaction between ANG II and GTN. Attenuation of the effect of GTN by ANG II disappeared after the single dose of Candesartan. In summary, subpressor dose of ANG II attenuated the effect of GTN. There was a lack of effect of ANG II in the presence of either vitamin C or Candesartan. Our results suggest that ANG II may stimulate superoxide production through AT1 receptor which inactivates NO by forming peroxynitrite.

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Role of Angiotensin Type-1 and Angiotensin Type-2 Receptors in the Expression of Vascular Integrins in Angiotensin II–Infused Rats

Hypertension ◽

10.1161/01.hyp.0000196272.79321.11 ◽

2006 ◽

Vol 47 (1) ◽

pp. 122-127 ◽

Cited By ~ 15

Author(s):

Pascal Brassard ◽

Farhad Amiri ◽

Gaétan Thibault ◽

Ernesto L. Schiffrin

Keyword(s):

Angiotensin Ii ◽

Angiotensin Type

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The Potential Association between the Risk of Post-Surgical Adhesion and the Activated Local Angiotensin II Type 1 Receptors: Need for Novel Treatment Strategies

Gastrointestinal Tumors ◽

10.1159/000514614 ◽

2021 ◽

pp. 1-8

Author(s):

Mahmood Tavakkoli ◽

Saeed Aali ◽

Borzoo Khaledifar ◽

Gordon A. Ferns ◽

Majid Khazaei ◽

...

Keyword(s):

Angiotensin Ii ◽

Molecular Mechanisms ◽

Transforming Growth Factor ◽

Therapeutic Potential ◽

Angiotensin Receptor Blockers ◽

Surgical Techniques ◽

Treatment Strategies ◽

Transforming Growth Factor Β

Background: Post-surgical adhesion bands (PSABs) are a common complication after abdominal or pelvic surgeries for different reasons like cancer treatment. Despite improvements in surgical techniques and the administration of drugs or the use of physical barriers, there has only been limited improvement in the frequency of postoperative adhesions. Complications of PSAB are pain, infertility, intestinal obstruction, and increased mortality. The most important molecular mechanisms for the development of PSAB are inflammatory response, oxidative stress, and overexpression of pro-fibrotic molecules such as transforming growth factor β. However, questions remain about the pathogenesis of this problem, for example, the causes for individual differences or why certain tissue sites are more prone to post-surgical adhesions. Summary: Addressing the pathological causes of PSAB, the potential role of local angiotensin II/angiotensin II type 1 receptors (AngII/AT1R), may help to prevent this problem. Key Message: The objective of this article was to explore the role of the AngII/AT1R axis potential to induce PSAB and the therapeutic potential of angiotensin receptor blockers in the prevention and treatment of PSAB.

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Critical Role of Bone Marrow Angiotensin II Type 1 Receptor in the Pathogenesis of Atherosclerosis in Apolipoprotein E–Deficient Mice

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvbaha.107.152363 ◽

2008 ◽

Vol 28 (1) ◽

pp. 90-96 ◽

Cited By ~ 49

Author(s):

Daiju Fukuda ◽

Masataka Sata ◽

Nobukazu Ishizaka ◽

Ryozo Nagai

Keyword(s):

Bone Marrow ◽

Angiotensin Ii ◽

Apolipoprotein E ◽

Critical Role ◽

Deficient Mice

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Reactive Oxygen Species-Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor Mrna by Angiotensin II

Hypertension ◽

10.1161/hyp.36.suppl_1.688-b ◽

2000 ◽

Vol 36 (suppl_1) ◽

pp. 688-688

Author(s):

Toshihiro Ichiki ◽

Kotaro Takeda ◽

Akira Takeshita

Keyword(s):

Reactive Oxygen Species ◽

Angiotensin Ii ◽

Nadph Oxidase ◽

Mrna Expression ◽

Crucial Role ◽

Oxygen Species ◽

Ang Ii ◽

Stimulation Of

58 Recent studies suggest a crucial role of reactive oxygen species (ROS) for the signaling of Angiotensin II (Ang II) through type 1 Ang II receptor (AT1-R). However, the role of ROS in the regulation of AT1-R expression has not been explored. In this study, we examined the effect of an antioxidant on the homologous downregulation of AT1-R by Ang II. Ang II (10 -6 mol/L) decreased AT1-R mRNA with a peak suppression at 6 hours of stimulation in rat aortic vascular smooth muscle cells (VSMC). Ang II dose-dependently (10 -8 -10 -6 ) suppressed AT1-R mRNA at 6 hours of stimulation. Preincubation of VSMC with N-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT1-R mRNA. The effect of NAC was due to stabilization of the AT1-R mRNA that was destabilized by Ang II. Ang II did not affect the promoter activity of AT1-R gene. Diphenylene iodonium (DPI), an inhibitor of NADH/NADPH oxidase failed to inhibit the Ang II-induced AT1-R mRNA downregulation. The Ang II-induced AT1-R mRNA downregulation was also blocked by PD98059, an extracellular signal-regulated protein kinase (ERK) kinase inhibitor. Ang II-induced ERK activation was inhibited by NAC as well as PD98059 whereas DPI did not inhibit it. To confirm the role of ROS in the regulation of AT1-R mRNA expression, VSMC were stimulated with H 2 O 2 . H 2 O 2 suppressed the AT1-R mRNA expression and activated ERK. These results suggest that production of ROS and activation of ERK are critical for downregulation of AT1-R mRNA. The differential effect of NAC and DPI on the downregulation of AT1-R mRNA may suggest the presence of other sources than NADH/NADPH oxidase pathway for ROS in Ang II signaling. Generation of ROS through stimulation of AT1-R not only mediates signaling of Ang II but may play a crucial role in the adaptation process of AT1-R to the sustained stimulation of Ang II.

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