Angiotensin II Type 2 Receptor Blockade Partially Negates Antihypertrophic Effects of Type 1 Receptor Blockade on Pressure-Overload Rat Cardiac Hypertrophy.

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.

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Combined Angiotensin II Type 1 and Type 2 Receptor Blockade on Vascular Remodeling and Matrix Metalloproteinases in Resistance Arteries

Hypertension ◽

10.1161/01.hyp.0000176744.15592.7d ◽

2005 ◽

Vol 46 (3) ◽

pp. 598-606 ◽

Cited By ~ 72

Author(s):

Pascal Brassard ◽

Farhad Amiri ◽

Ernesto L. Schiffrin

Keyword(s):

Angiotensin Ii ◽

Matrix Metalloproteinases ◽

Vascular Remodeling ◽

Receptor Blockade ◽

Resistance Arteries

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

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/hq0102.102277 ◽

2002 ◽

Vol 22 (1) ◽

pp. 49-54 ◽

Cited By ~ 58

Author(s):

Lan Wu ◽

Masaru Iwai ◽

Hironori Nakagami ◽

Rui Chen ◽

Jun Suzuki ◽

...

Keyword(s):

Angiotensin Ii ◽

Cardiac Remodeling ◽

Receptor Blockade

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

Pharmaceuticals ◽

10.3390/ph14050469 ◽

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.

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Comparison of angiotensin II type 1-receptor blockers to regress pressure overload-induced cardiac hypertrophy in mice

Hypertension Research ◽

10.1038/hr.2010.182 ◽

2010 ◽

Vol 33 (12) ◽

pp. 1289-1297 ◽

Cited By ~ 38

Author(s):

Lei Li ◽

Ning Zhou ◽

Hui Gong ◽

Jian Wu ◽

Li Lin ◽

...

Keyword(s):

Angiotensin Ii ◽

Cardiac Hypertrophy ◽

Pressure Overload ◽

Receptor Blockers

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Thyroid Hormone Increases TGF-β1 in Cardiomyocytes Cultures Independently of Angiotensin II Type 1 and Type 2 Receptors

International Journal of Endocrinology ◽

10.1155/2010/384890 ◽

2010 ◽

Vol 2010 ◽

pp. 1-7 ◽

Cited By ~ 3

Author(s):

Gabriela Placoná Diniz ◽

Marcela Sorelli Carneiro-Ramos ◽

Maria Luiza Morais Barreto-Chaves

Keyword(s):

Angiotensin Ii ◽

Cardiac Hypertrophy ◽

Transforming Growth Factor ◽

Cardiac Fibroblasts ◽

Angiotensin Ii Receptors ◽

Cardiomyocyte Hypertrophy ◽

Tgf Β1

TH-induced cardiac hypertrophyin vivois accompanied by increased cardiac Transforming Growth Factor-β1 (TGF-β1) levels, which is mediated by Angiotensin II type 1 receptors (AT1R) and type 2 receptors (AT2R). However, the possible involvement of this factor in TH-induced cardiac hypertrophy is unknown. In this study we evaluated whether TH is able to modulate TGF-β1 in isolated cardiac, as well as the possible contribution of AT1R and AT2R in this response. The cardiac fibroblasts treated withT3did not show alteration on TGF-β1 expression. However, cardiomyocytes treated withT3presented an increase in TGF-β1 expression, as well as an increase in protein synthesis. The AT1R blockade prevented theT3-induced cardiomyocyte hypertrophy, while the AT2R blockage attenuated this response. TheT3-induced increase on TGF-β1 expression in cardiomyocytes was not changed by the use of AT1R and AT2R blockers. These results indicate that Angiotensin II receptors are not implicated inT3-induced increase on TGF-βexpression and suggest that the trophic effects exerted byT3on cardiomyocytes are not dependent on the higher TGF-β1 levels, since the AT1R and AT2R blockers were able to attenuate theT3-induced cardiomyocyte hypertrophy but were not able to attenuate the increase on TGF-β1 levels promoted byT3.

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