Irisin lowers blood pressure in Zucker diabetic rats by regulating the functions of renal angiotensin II type 1 receptor via the inhibition of the NF-κB signaling pathway

Peptides ◽  
2022 ◽  
Vol 147 ◽  
pp. 170688
Author(s):  
Yu Huang ◽  
Qin Chen ◽  
Qiong Jiang ◽  
Ziwen Zhao ◽  
Jun Fang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Signaling Pathway ◽  
Diabetic Rats

scholarly journals Chronic NF-κB blockade improves renal angiotensin II type 1 receptor functions and reduces blood pressure in Zucker diabetic rats

2015 ◽  
Vol 14 (1) ◽  
Author(s):  
Hao Luo ◽  
Xinquan Wang ◽  
Jialiang Wang ◽  
Caiyu Chen ◽  
Na Wang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Diabetic Rats

scholarly journals Mitochondrial angiotensin II receptors regulate oxygen consumption in kidney mitochondria from healthy and type 1 diabetic rats

2020 ◽  
Vol 318 (3) ◽  
pp. F683-F688 ◽  
Author(s):  
Malou Friederich-Persson ◽  
Patrik Persson
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Diabetic Rats ◽  
Kidney Cortex ◽  
Ang Ii ◽  
Kidney Mitochondria ◽  
Receptor Inhibition

Exaggerated activation of the renin-angiotensin-aldosterone system (RAAS) is a key feature in diseases such as hypertension, diabetes, and chronic kidney disease. Recently, an intracellular RAAS was demonstrated with angiotensin II (ANG II) type 1 (AT1) and type 2 (AT2) receptors expressed in nuclei and mitochondria. Diabetes is associated with both mitochondrial dysfunction and increased intracellular ANG II concentration in the kidney cortex. The present study investigated the role of ANG II signaling in kidney cortex mitochondria isolated from control and streptozotocin-induced diabetic rats. Mitochondrial oxygen consumption was evaluated after addition of ANG II alone or after preincubation with candesartan (AT1 receptor antagonist), PD-123319 (AT2 receptor antagonist), or the two in combination. ANG II binds to only mitochondrial AT2 receptors in control rats and both AT1 receptors and AT2 receptors in diabetic rats. ANG II decreased oxygen consumption in mitochondria from both control and diabetic rats. ANG II response was reversed to increased oxygen consumption by the nitric oxide synthase inhibitor N-nitro-l-arginine methyl ester. AT1 receptor inhibition did not affect the response to ANG II, whereas AT2 receptor inhibition abolished the response in mitochondria from control rats and reversed the response to increased oxygen consumption through superoxide-induced mitochondrial uncoupling in mitochondria from diabetic rats. ANG II decrease mitochondrial respiration via AT2 receptor-mediated nitric oxide release in both control and diabetic rats. AT1 receptors do not regulate mitochondria function in control rats, whereas ANG II via AT1 receptors increase mitochondria leak respiration in diabetic animals.

scholarly journals Addition of a Nitric Oxide Donor to an Angiotensin II Type 1 Receptor Blocker May Cancel Its Blood Pressure-Lowering Effects

2015 ◽  
Vol 56 (6) ◽  
pp. 656-660 ◽  
Author(s):  
Eiji Yahiro ◽  
Shin-ichiro Miura ◽  
Yasunori Suematsu ◽  
Yoshino Matsuo ◽  
Tadaaki Arimura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Receptor Blocker ◽  
Nitric Oxide Donor ◽  
Blood Pressure Lowering ◽  
Pressure Lowering

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

scholarly journals Curcumin decreases renal triglyceride accumulation through AMPK–SREBP signaling pathway in streptozotocin-induced type 1 diabetic rats

2013 ◽  
Vol 24 (5) ◽  
pp. 796-802 ◽  
Author(s):  
Vivian Soetikno ◽  
Flori R. Sari ◽  
Vijayakumar Sukumaran ◽  
Arun Prasath Lakshmanan ◽  
Meilei Harima ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Diabetic Rats ◽  
Triglyceride Accumulation

ANG II enhances contractile responses via PI3-kinase p110δ pathway in aortas from diabetic rats with systemic hyperinsulinemia

2006 ◽  
Vol 291 (2) ◽  
pp. H846-H853 ◽  
Author(s):  
Tsuneo Kobayashi ◽  
Yuko Hayashi ◽  
Kumiko Taguchi ◽  
Takayuki Matsumoto ◽  
Katsuo Kamata
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Chronic Administration ◽  
Diabetic Rats ◽  
Ang Ii ◽  
Phosphatidylinositol 3 Kinase ◽  
Contractile Responses ◽  
Vascular Contractility ◽  
K Activity

We investigated the involvement of ANG II and phosphatidylinositol 3-kinase (PI3-K) in the enhanced aortic contractile responses induced by hyperinsulinemia in chronic insulin-treated Type 1 diabetic rats. Plasma ANG II levels were elevated in untreated compared with control diabetic rats and further increased in insulin-treated diabetic rats. Aortic contractile responses and systolic blood pressure were significantly enhanced in chronic insulin-treated diabetic rats compared with the other groups. These insulin-induced increases were largely prevented by cotreatment with losartan (an ANG II type 1 receptor antagonist) or enalapril (an angiotensin-converting enzyme inhibitor). LY-294002 (a PI3-K inhibitor) diminished the increases in contractile responses in ANG II-incubated aortas and aortas from chronic insulin-treated diabetic rats. The norepinephrine (NE)-stimulated levels of p110δ-associated PI3-K activity and p110δ protein expression were increased in aortas from insulin-treated diabetic compared with control and untreated diabetic rats, and chronic administration of losartan blunted these increases. Contractions were significantly larger in aortas from diabetic rats incubated with a low concentration (inducing ∼10% of the maximum contraction) of ANG II or with NE or isotonic K+ than in aortas from nonincubated diabetic rats. NE-stimulated p110 PI3-K activity was elevated in aortas from diabetic rats coincubated with a noncontractile dose of ANG II. These results suggest that, in insulin-treated Type 1 diabetic rats with hyperinsulinemia, chronic ANG II type 1 receptor blockade blunts the increases in vascular contractility and blood pressure via a decrease in p110δ-associated PI3-K activity.

scholarly journals Angiotensin II stimulates canonical TGF-β signaling pathway through angiotensin type 1 receptor to induce granulation tissue contraction

2014 ◽  
Vol 93 (3) ◽  
pp. 289-302 ◽  
Author(s):  
Tosan Ehanire ◽  
Licheng Ren ◽  
Jennifer Bond ◽  
Manuel Medina ◽  
George Li ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Signaling Pathway ◽  
Granulation Tissue ◽  
Tissue Contraction ◽  
Angiotensin Type

Angiotensin II downregulates ACE2-mediated enhancement of MMP-2 activity in human cardiofibroblasts

2013 ◽  
Vol 91 (6) ◽  
pp. 435-442 ◽  
Author(s):  
Tang-Ching Kuan ◽  
Mu-Yuan Chen ◽  
Yan-Chiou Liao ◽  
Li Ko ◽  
Yi-Han Hong ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Signaling Pathway ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Lentiviral Infection ◽  
And Control

Angiotensin converting enzyme II (ACE2) is a component of the renin-angiotensin system (RAS) that negatively regulates angiotensin II (Ang II). Ang II, in turn, affects the expression of matrix metalloproteinases (MMPs) to induce heart remodeling. The specific mechanisms by which ACE2 regulates MMP-2, however, remain unclear. The aim of this study was to investigate the regulatory relationships between Ang II, ACE2, and MMP-2. ACE2 expression was upregulated and downregulated in human cardiofibroblasts (HCFs) by lentiviral infection. Effects on MMP-2 activity, shed ACE2 activity, extracellular signal-regulated kinase (ERK) signaling pathway, and ADAM metallopeptidase domain 17 (ADAM17) expression were assessed. ACE2 increased MMP-2 activity, and Ang II inhibited this effect through the Ang II type-1 receptor (AT1R) and ERK1/2 signaling pathway. Ang II also reduced the effect of ACE2 on ERK1/2 levels, the activity of shed ACE2, and adam17 expression in HCFs. Additionally, these Ang II-mediated reductions could be attenuated by AT1R antagonist valsartan. In conclusion, these data help to clarify how ACE2 and Ang II interact to regulate MMP-2 and control tissue remodeling in heart disease.

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