New evidence for vascular interactions between aldosterone, angiotensin II and antioxidants in isolated smooth muscle cells of rats

Open Medicine ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. 704-712
Author(s):  
Raducu Popescu ◽  
Walther Bild ◽  
Alin Ciobica ◽  
Veronica Bild
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cells ◽  
Nitrosative Stress ◽  
Reactive Oxygen ◽  
Muscle Cells ◽  
No Production ◽  
Nitrogen Species ◽  
First Case

AbstractAccumulating evidence suggests that the nongenomic cardiovascular actions of aldosterone are produced by varied cellular pathways and mediated by a multitude of messenger systems including the reactive oxygen and nitrogen species. Considering the involvement of the oxidative and nitrosative stress in the pathways leading to the activation of the angiotensin — aldosterone system, in the current study we tried to evaluate the functional interactions between aldosterone, angiotensin II and antioxidants in isolated vascular smooth muscle of aortic rings from rats. Our data provide additional arguments that the nongenomic actions of aldosterone on aortic smooth muscle cells of rats are a question of cross-talk and balance between its rapid vasoconstrictor and vasodilator effects, as result of the activation of reactive oxygen species in the first case and of nitrogen species in the second. In this way, it seems that at low ambient oxidative stress, aldosterone promotes nitric oxide (NO) production and vasodilatation, while in situations with increased oxidative stress the endothelial dysfunction and detrimental effects induced by vasoconstriction will prevail. Thus, aldosterone could be considered both “friend and foe”. This could be relevant for the ways in which aldosterone damages cardiovascular functions and could lead to significant therapeutic improvements.

Blackberry, raspberry and black raspberry polyphenol extracts attenuate angiotensin II-induced senescence in vascular smooth muscle cells

2016 ◽  
Vol 7 (10) ◽  
pp. 4175-4187 ◽  
Author(s):  
Rafaela G. Feresin ◽  
Jingwen Huang ◽  
DawnKylee S. Klarich ◽  
Yitong Zhao ◽  
Shirin Pourafshar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Black Raspberry

Blackberry, raspberry and black raspberry polyphenols reduce angiotensin II-induced oxidative stress and senescence of vascular smooth muscle cells.

Angiotensin II stimulates the production of NO and peroxynitrite in endothelial cells

1998 ◽  
Vol 274 (1) ◽  
pp. C214-C220 ◽  
Author(s):  
Maria E. Pueyo ◽  
Jean-François Arnal ◽  
Jacques Rami ◽  
Jean-Baptiste Michel
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
No Synthase ◽  
No Production ◽  
Ang Ii ◽  
Calmodulin Antagonist ◽  
Enhanced Chemiluminescence

Angiotensin II (ANG II) produces vasoconstriction by a direct action on smooth muscle cells via AT1 receptors. These receptors are also present in the endothelium, but their function is poorly understood. This study was therefore undertaken to determine whether ANG II elicits the release of nitric oxide (NO) from cultured rat aortic endothelial cells. NO production, measured by the accumulation of nitrite and nitrate, was enhanced by 10−7 M ANG II. The biological activity of the NO released by ANG II action was evaluated by measuring its guanylate cyclase-stimulating activity in smooth muscle cells. The guanosine 3′,5′-cyclic monophosphate (cGMP) content of smooth muscle cells was significantly increased by exposure of supernatant from ANG II-stimulated endothelial cells. These effects resulted from the activation of NO synthase, as they were inhibited by the l-arginine analogs. These ANG II actions were mediated by the AT1 receptor, as shown by their inhibition by the AT1 antagonist losartan. The cGMP production by reporter cells was inhibited by the calmodulin antagonist W-7, suggesting that ANG II activates endothelial calmodulin-dependent NO synthase. This hypothesis is also supported by the increase of intracellular free calcium induced by ANG II in endothelial cells. ANG II also stimulated luminol-enhanced chemiluminescence in endothelial cells. This effect was inhibited by N ω-monomethyl-l-arginine and superoxide dismutase, suggesting that this luminol-enhanced chemiluminescence reflected an increase in peroxynitrite production. Thus ANG II stimulates NO release from macrovascular endothelium, which may modulate the direct vasoconstrictor effect of ANG II on smooth muscle cells. However, this beneficial effect may be counteracted by the simultaneous production of peroxynitrite, which could contribute to several pathological processes in the vascular wall.

Hydrogen peroxide mediates a transient vasorelaxation with tempol during oxidative stress

2007 ◽  
Vol 293 (4) ◽  
pp. H2085-H2092 ◽  
Author(s):  
Yifan Chen ◽  
Adam Pearlman ◽  
Zaiming Luo ◽  
Christopher S. Wilcox
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Prolonged Exposure ◽  
Muscle Cells ◽  
Mesenteric Arteries

Tempol catalyzes the formation of H2O2 from superoxide and relaxes blood vessels. We tested the hypothesis that the generation of H2O2 by tempol in vascular smooth muscle cells during oxidative stress contributes to the vasorelaxation. Tempol and nitroblue tetrazolium (NBT) both metabolize superoxide in vascular smooth muscle cells, but only tempol generates H2O2. Rat pressurized mesenteric arteries were exposed for 20 min to the thromboxane-prostanoid receptor agonist, U-46619, or norepinephrine. During U-46619, tempol caused a transient dilation (22 ± 2%), whereas NBT was ineffective (2 ± 1%), and neither dilated vessels constricted with norepinephrine, which does not cause vascular oxidative stress. Neither endothelium removal nor blockade of K+ channels with 40 mM KCl affected the tempol-induced dilation, but catalase blunted the tempol dilation by 53 ± 7%. Tempol, but not NBT, increased H2O2 in rat mesenteric vessels detected with dichlorofluorescein. To test physiological relevance in vivo, topical application of tempol caused a transient dilation (184 ± 20%) of mouse cremaster arterioles exposed to angiotensin II for 30 min, which was not seen with NBT (9 ± 4%). The vasodilation to tempol was reduced by 68 ± 6% by catalase. We conclude that the transient relaxation of blood vessels by tempol after prolonged exposure to U-46619 or angiotensin II is mediated in part via production of H2O2 and is largely independent of the endothelium and potassium channels.

scholarly journals Sirt3 Protects Against Thoracic Aortic Dissection Formation by Reducing Reactive Oxygen Species, Vascular Inflammation, and Apoptosis of Smooth Muscle Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
Lin Qiu ◽  
Shaolei Yi ◽  
Tingting Yu ◽  
Yan Hao
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Aortic Dissection ◽  
Smooth Muscle Cells ◽  
Vascular Inflammation ◽  
Reactive Oxygen ◽  
Muscle Cells ◽  
Oxygen Species ◽  
Thoracic Aortic Dissection

Sirtuin3 (Sirt3) is a histone deacetylase involved in the regulation of many cellular processes. Sirt3 deficiency is known to increase oxidative stress. Reactive oxygen species (ROS) promote degradation of the extracellular matrix and vascular smooth muscle cell (VSMC) apoptosis. Reducing oxidative stress by Sirt3 overexpression could have therapeutic potential for limiting thoracic aortic dissection (TAD) development. We hypothesized that Sirt3 deficiency could increase the risk for TAD by decreasing ROS elimination and that Sirt3 overexpression (Sirt3OE) could provide an alternative option for TAD treatment. Mice with TAD had significantly lower Sirt3 expression than normal subjects. Sirt3 KO mice exhibit significantly increased TAD incidence rate and increased aortic diameters. Moreover, Sirt3 overexpression reduced Ang II-induced ROS production, NF-kB activation, and apoptosis in human aortic smooth muscle cells (HASMCs). Sirt3 overexpression attenuated aneurysm formation and decreased aortic expansion. In conclusion, our data showed that Sirt3 deficiency increases susceptibility to TAD formation by attenuating anti-ROS effects and increasing VSMC apoptosis and vascular inflammation.

scholarly journals Pressure Promotes Angiotensin II–Mediated Migration of Human Coronary Smooth Muscle Cells Through Increase in Oxidative Stress

Hypertension ◽  
2002 ◽  
Vol 39 (2) ◽  
pp. 433-437 ◽  
Author(s):  
Kenichi Yasunari ◽  
Kensaku Maeda ◽  
Munehiro Nakamura ◽  
Junichi Yoshikawa
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Coronary Smooth Muscle
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