scholarly journals Hypertension and Angiotensin II Hypersensitivity in Aminopeptidase A—deficient Mice

2003 ◽  
Vol 9 (1-2) ◽  
pp. 57-62 ◽  
Author(s):  
Takashi Mitsui ◽  
Seiji Nomura ◽  
Mayumi Okada ◽  
Yasumasa Ohno ◽  
Honami Kobayashi ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Aminopeptidase A ◽  
Deficient Mice

Lack of angiotensin II conversion to angiotensin III increases water but not alcohol consumption in aminopeptidase A-deficient mice

2006 ◽  
Vol 136 (1-3) ◽  
pp. 130-137 ◽  
Author(s):  
Franziska Faber ◽  
Florian Gembardt ◽  
Xiaoou Sun ◽  
Shigehiko Mizutani ◽  
Wolf-Eberhard Siems ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Alcohol Consumption ◽  
Angiotensin Iii ◽  
Aminopeptidase A ◽  
Deficient Mice

scholarly journals Albuminuria in Mice after Injection of Antibodies against Aminopeptidase A: Role of Angiotensin II

2001 ◽  
Vol 12 (12) ◽  
pp. 2711-2720
Author(s):  
Miriam E. Gerlofs-Nijland ◽  
Karel J. M. Assmann ◽  
Henry B. P. M. Dijkman ◽  
Jürgen W.C. Dieker ◽  
Jacco P. H. F. van Son ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Inflammatory Cells ◽  
Coagulation System ◽  
Ang Ii ◽  
Kidney Morphology ◽  
Aminopeptidase A ◽  
Deficient Mice

ABSTRACT. It has been shown that injection of combinations of anti-aminopeptidase A (APA) monoclonal antibodies (mAb) that inhibit the enzyme activity induces an acute albuminuria in mice. This albuminuria is not dependent on inflammatory cells, complement, or the coagulation system. APA is an important regulator of the renin-angiotensin system because it is involved in the degradation of angiotensin II (Ang II). This study examined the potential role of glomerular Ang II in the induction of albuminuria. The relation among renal Ang II, glomerular APAX enzyme activity, and albuminuria was examined first. Injection of the nephritogenic combinations ASD-3/37 and ASD-37/41 in BALB/c mice induced albuminuria, whereas the non-nephritogenic combination ASD-3/41 had no effect. There was no clear relation between the inhibition of glomerular APA activity and albuminuria, yet it was evident that intrarenal Ang II levels were significantly increased in albuminuric mice and not in nonalbuminuric mice. As a next step, anti-APA mAb were administered to angiotensinogen-deficient mice that do not produce Ang II, and kidney morphology and albuminuria were determined. Angiotensinogen-deficient mice also developed albuminuria upon ASD-37/41 administration. Altogether, these findings clearly demonstrate that Ang II is not required for the induction of albuminuria upon injection of enzyme-inhibiting anti-APA mAb.

Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

2008 ◽  
Vol 57 (2) ◽  
pp. 84-91 ◽  
Author(s):  
K. Katada ◽  
N. Yoshida ◽  
T. Suzuki ◽  
T. Okuda ◽  
K. Mizushima ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Colonic Inflammation ◽  
Deficient Mice

Angiotensin II infusion induces site-specific intra-laminar hemorrhage in macrophage colony-stimulating factor-deficient mice

2006 ◽  
Vol 186 (2) ◽  
pp. 282-290 ◽  
Author(s):  
Fjoralba Babamusta ◽  
Debra L. Rateri ◽  
Jessica J. Moorleghen ◽  
Deborah A. Howatt ◽  
Xiang-An Li ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Colony Stimulating Factor ◽  
Site Specific ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Deficient Mice

Placental Aminopeptidase A as a Possible Barrier of Angiotensin II between Mother and Fetus

Placenta ◽  
2000 ◽  
Vol 21 (7) ◽  
pp. 621-627 ◽  
Author(s):  
Y. Hariyama ◽  
A. Itakura ◽  
M. Okamura ◽  
M. Ito ◽  
Y. Murata ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Aminopeptidase A

scholarly journals Mesenchymal stem cells attenuate angiotensin II-induced aortic aneurysm growth in apolipoprotein E-deficient mice

2011 ◽  
Vol 54 (6) ◽  
pp. 1743-1752 ◽  
Author(s):  
Ryotaro Hashizume ◽  
Aika Yamawaki-Ogata ◽  
Yuichi Ueda ◽  
William R. Wagner ◽  
Yuji Narita
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Apolipoprotein E ◽  
Aneurysm Growth ◽  
Deficient Mice

Embryonic lethality in Dear gene-deficient mice: new player in angiogenesis

2005 ◽  
Vol 23 (3) ◽  
pp. 257-268 ◽  
Author(s):  
Victoria L. M. Herrera ◽  
Lorenz R. B. Ponce ◽  
Pia D. Bagamasbad ◽  
Benjamin D. VanPelt ◽  
Tamara Didishvili ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Embryonic Lethality ◽  
Female Rats ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Angiotensin Ii Receptor ◽  
Endothelin 1 ◽  
Receptor Isoforms ◽  
Age Range ◽  
Deficient Mice

The dual endothelin-1/angiotensin II receptor (Dear) binds endothelin-1 (ET-1) and angiotensin II (ANG II) with equal affinities in the Dahl S/JRHS rat strain. To elucidate its physiological significance within the context of multiple receptor isoforms and diverse ET-1 and ANG II functions spanning blood pressure regulation, tumor proliferation, and angiogenesis, we characterized mouse Dear and Dear-deficient mice. Unlike null mutant models of ET-1, ANG II, and all other ET-1 and ANG II receptors, Dear−/− deficiency results in impaired angiogenesis, dysregulated neuroepithelial development, and embryonic lethality by embryonic day 12.5. Interestingly, mouse Dear does not bind ANG II, similar to Dahl R/JRHS rat Dear, but binds ET-1 and vascular endothelial growth factor (VEGF) signal peptide (VEGFsp) with equal affinities, suggesting a putative novel multifunction for VEGFsp and a parsimonious mechanism for coordination of VEGF-induced and Dear-mediated pathways. Consistent with its developmental angiogenic role, Dear inhibition results in decreased tumor growth in B16-F10 melanoma cell-induced subcutaneous tumor in female Dear+/−/C57BL6BC10 mice, but not in males (age 3.5 mo), and in 127Cs radiation-induced orthotopic mammary tumors in Sprague-Dawley female rats (age range 3–6.5 mo). Altogether, the data identify Dear as a new player in angiogenesis during development downstream to, and nonredundant with, VEGF-mediated pathways, as well as a putative modulator of tumor angiogenesis acting within a gender-specific paradigm.

Abstract P363: Annexin-A1 Deficiency Exaggerates Cardiac Remodeling In Angiotensin II-induced Hypertension

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Kristy Jackson ◽  
Jaideep Singh ◽  
Yen Zhi Ng ◽  
Cheng Peng ◽  
Anida Velagic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cardiac Remodeling ◽  
Physiological Role ◽  
Preclinical Model ◽  
Annexin A1 ◽  
Ang Ii ◽  
Cardiac Damage ◽  
Induced Hypertension ◽  
Deficient Mice

Introduction: We have previously demonstrated that the naturally-occurring anti-inflammatory and pro-resolving protein Annexin-A1 (Anx-A1) limits the acute inflammatory response post myocardial infarction, but its impact on chronic inflammation, such as hypertension, has not been explored. This study aims to investigate the role of Anx-A1 in a preclinical model of hypertension, induced by angiotensin-II (Ang-II). Methods: 15-week-old male C57BL/6 or ANXA1 -/- were anesthetized (isoflurane, 2-4% v/v) and implanted with an osmotic minipump randomly assigned to receive Ang-II (0.7mg/kg/day) or vehicle (saline). Radiotelemetry recordings of blood pressure were taken at 10 intermittent timepoints from baseline to the end of the 29-day infusion period. Animals were euthanized with pentobarbitone (100mg/kg; i.p.) at endpoint and organ weights recorded and normalized to bodyweight. Left ventricle (LV) samples were stained with picrosirius red to assess total LV collagen deposition. Results: Ang II-induced mice at the end of the study had elevated mean arterial pressure (MAP), cardiac hypertrophy and fibrosis compared to normotensive mice (Table). Anx-A1 deficient mice given Ang II had an even greater increase in MAP and cardiac remodeling compared to WT. Interestingly, MAP of Anx-A1 deficient mice at baseline is significantly higher compare to C57BL/6 counterparts (Table). Conclusion: This is the first study to demonstrate that deficiency of Anx-A1 exaggerates cardiac remodeling in AngII-induced hypertension, suggesting that endogenous Anx-A1 might play previously unappreciated physiological role in regulating blood pressure. This supports the development of Anx-A1 based pharmacotherapy against hypertension-induced cardiac damage.

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