scholarly journals Roles of Angiotensin II Type 2 Receptor Stimulation Associated With Selective Angiotensin II Type 1 Receptor Blockade With Valsartan in the Improvement of Inflammation-Induced Vascular Injury

Circulation ◽  
2001 ◽  
Vol 104 (22) ◽  
pp. 2716-2721 ◽  
Author(s):  
Lan Wu ◽  
Masaru Iwai ◽  
Hironori Nakagami ◽  
Zhen Li ◽  
Rui Chen ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Vascular Injury ◽  
Receptor Blockade ◽  
Receptor Stimulation

Angiotensin II type 1 receptor blockade attenuates renal fibrogenesis in an immune-mediated nephritic kidney through counter-activation of angiotensin II type 2 receptor

2004 ◽  
Vol 314 (2) ◽  
pp. 403-408 ◽  
Author(s):  
Hirokazu Okada ◽  
Yusuke Watanabe ◽  
Tsutomu Inoue ◽  
Tatsuya Kobayashi ◽  
Tomohiro Kikuta ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Blockade ◽  
Immune Mediated ◽  
Renal Fibrogenesis

scholarly journals Regulation of Vascular Proteoglycan Synthesis by Angiotensin II Type 1 and Type 2 Receptors

2001 ◽  
Vol 12 (12) ◽  
pp. 2609-2615
Author(s):  
Ryoko Shimizu-Hirota ◽  
Hiroyuki Sasamura ◽  
Mizuo Mifune ◽  
Hideaki Nakaya ◽  
Mari Kuroda ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Proteoglycan Synthesis ◽  
At2 Receptor ◽  
Receptor Stimulation ◽  
Epidermal Growth

ABSTRACT. Recent studies have shown that proteoglycans play an important role in the development of vascular disease and renal failure. In this study, the effects of angiotensin II (AngII) type 1 (AT1) and type 2 (AT2) receptor stimulation on glycosaminoglycan and proteoglycan core protein synthesis in vascular smooth muscle cells (VSMC) were examined. Treatment of AT1 receptor-expressing VSMC with AngII resulted in a dose-dependent and time-dependent increase (2- to 4-fold) in 3H-glucosamine/35S-sulfate incorporation, which was abolished by pretreatment with the AT1 receptor antagonist, losartan. The effects of AngII were inhibited by the epidermal growth factor receptor inhibitor, AG1478, and the mitagen-activated protein kinase kinase inhibitor, PD98059, but not the protein kinase C inhibitors, chelerythrine and staurosporine. AngII treatment also resulted in significant increases in the mRNA of the core proteins, versican, biglycan, and perlecan. The effects of AT2 receptor stimulation were examined by retroviral transfection of VSMC with the AT2 receptor. Stimulation of the AT2 receptor in these VSMC-AT2 cells resulted in a significant (1.3-fold) increase in proteoglycan synthesis, which was abolished by the AT2 receptor antagonist, PD123319, and attenuated by pretreatment with pertussis toxin. These results implicate both AT1 and AT2 receptors in the regulation of proteoglycan synthesis and suggest the involvement of epidermal growth factor receptor-dependent tyrosine kinase pathways and Gαi/o-mediated mechanisms in the effects of the two receptors.

scholarly journals A Possible Anti-Inflammatory Role of Angiotensin II Type 2 Receptor in Immune-Mediated Glomerulonephritis during Type 1 Receptor Blockade

2006 ◽  
Vol 169 (5) ◽  
pp. 1577-1589 ◽  
Author(s):  
Hirokazu Okada ◽  
Tsutomu Inoue ◽  
Tomohiro Kikuta ◽  
Yusuke Watanabe ◽  
Yoshihiko Kanno ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Blockade ◽  
Immune Mediated ◽  
Anti Inflammatory

Angiotensin II mediates uterine vasoconstriction through α-stimulation

2004 ◽  
Vol 287 (1) ◽  
pp. H126-H134 ◽  
Author(s):  
Blair E. Cox ◽  
Timothy A. Roy ◽  
Charles R. Rosenfeld
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Pressor Responses ◽  
Adrenergic Activation

Intravenous angiotensin II (ANG II) increases uterine vascular resistance (UVR), whereas uterine intra-arterial infusions do not. Type 2 ANG II (AT2) receptors predominate in uterine vascular smooth muscle; this may reflect involvement of systemic type 1 ANG II (AT1) receptor-mediated α-adrenergic activation. To examine this, we compared systemic pressor and UVR responses to intravenous phenylephrine and ANG II without and with systemic or uterine α-receptor blockade and in the absence or presence of AT1 receptor blockade in pregnant and nonpregnant ewes. Systemic α-receptor blockade inhibited phenylephrine-mediated increases in mean arterial pressure (MAP) and UVR, whereas uterine α-receptor blockade alone did not alter pressor responses and resulted in proportionate increases in UVR and MAP. Although neither systemic nor uterine α-receptor blockade affected ANG II-mediated pressor responses, UVR responses decreased >65% and also were proportionate to increases in MAP. Systemic AT1 receptor blockade inhibited all responses to intravenous ANG II. In contrast, uterine AT1 receptor blockade + systemic α-receptor blockade resulted in persistent proportionate increases in MAP and UVR. Uterine AT2 receptor blockade had no effects. We have shown that ANG II-mediated pressor responses reflect activation of systemic vascular AT1 receptors, whereas increases in UVR reflect AT1 receptor-mediated release of an α-agonist and uterine autoregulatory responses.

scholarly journals Effect of Angiotensin II Type 1 Receptor Blockade on Cardiac Remodeling in Angiotensin II Type 2 Receptor Null Mice

2002 ◽  
Vol 22 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Lan Wu ◽  
Masaru Iwai ◽  
Hironori Nakagami ◽  
Rui Chen ◽  
Jun Suzuki ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Remodeling ◽  
Receptor Blockade

scholarly journals The Embryonic Chick Femur Organotypic Model as a Tool to Analyze the Angiotensin II Axis on Bone Tissue

2021 ◽  
Vol 14 (5) ◽  
pp. 469
Author(s):  
Thais Francini Garbieri ◽  
Victor Martin ◽  
Carlos Ferreira dos Santos ◽  
Pedro de Sousa Gomes ◽  
Maria Helena Fernandes
Keyword(s):  
Angiotensin Ii ◽  
Ex Vivo ◽  
Renin Angiotensin System ◽  
Bone Volume ◽  
Tissue Response ◽  
Data Availability ◽  
Receptor Blockade ◽  
Embryonic Chick

Activation of renin–angiotensin system (RAS) plays a role in bone deterioration associated with bone metabolic disorders, via increased Angiotensin II (AngII) targeting Angiotensin II type 1 receptor/Angiotensin II type 2 receptor (AT1R/AT2R). Despite the wide data availability, the RAS role remains controversial. This study analyzes the feasibility of using the embryonic chick femur organotypic model to address AngII/AT1R/AT2R axis in bone, which is an application not yet considered. Embryonic day-11 femurs were cultured ex vivo for 11 days in three settings: basal conditions, exposure to AngII, and modulation of AngII effects by prior receptor blockade, i.e., AT1R, AT2R, and AT1R + AT2R. Tissue response was evaluated by combining µCT and histological analysis. Basal-cultured femurs expressed components of RAS, namely ACE, AT1R, AT2R, and MasR (qPCR analysis). Bone formation occurred in the diaphyseal region in all conditions. In basal-cultured femurs, AT1R blocking increased Bone Surface/Bone Volume (BS/BV), whereas Bone Volume/Tissue Volume (BV/TV) decreased with AT2R or AT1R + AT2R blockade. Exposure to AngII greatly decreased BV/TV compared to basal conditions. Receptor blockade prior to AngII addition prevented this effect, i.e., AT1R blockade induced BV/TV, whereas blocking AT2R caused lower BV/TV increase but greater BS/BV; AT1R + AT2R blockade also improved BV/TV. Concluding, the embryonic chick femur model was sensitive to three relevant RAS research setups, proving its usefulness to address AngII/AT1R/AT2R axis in bone both in basal and activated conditions.

Angiotensin II modulates VEGF-driven angiogenesis by opposing effects of type 1 and type 2 receptor stimulation in the microvascular endothelium

2012 ◽  
Vol 24 (6) ◽  
pp. 1261-1269 ◽  
Author(s):  
Javier Carbajo-Lozoya ◽  
Susanne Lutz ◽  
Yuxi Feng ◽  
Jens Kroll ◽  
Hans-Peter Hammes ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Microvascular Endothelium ◽  
Receptor Stimulation ◽  
Opposing Effects
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