Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects

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• 作者：Takumi Sakurada (1)
  Keisuke Ishizawa (2)
  Masaki Imanishi (1)
  Yuki Izawa-Ishizawa (1)
  Shoko Fujii (2)
  Erika Tominaga (1)
  Teppei Tsuneishi (1)
  Yuya Horinouchi (1)
  Yoshitaka Kihira (1)
  Yasumasa Ikeda (1)
  Shuhei Tomita (1)
  Ken-ichi Aihara (3)
  Kazuo Minakuchi (4)
  Koichiro Tsuchiya (2)
  Toshiaki Tamaki (1)
  
• 关键词：Vascular remodeling ; Oxidative stress ; Vascular smooth muscle cells ; Angiotensin II ; Free radical scavengers
• 刊名：Naunyn-Schmiedeberg's Archives of Pharmacology
• 出版年：2013
• 出版时间：January 2013
• 年：2013
• 卷：386
• 期：1
• 页码：29-39
• 全文大小：602KB
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• 作者单位：Takumi Sakurada (1)
  Keisuke Ishizawa (2)
  Masaki Imanishi (1)
  Yuki Izawa-Ishizawa (1)
  Shoko Fujii (2)
  Erika Tominaga (1)
  Teppei Tsuneishi (1)
  Yuya Horinouchi (1)
  Yoshitaka Kihira (1)
  Yasumasa Ikeda (1)
  Shuhei Tomita (1)
  Ken-ichi Aihara (3)
  Kazuo Minakuchi (4)
  Koichiro Tsuchiya (2)
  Toshiaki Tamaki (1)
  
  1. Department of Pharmacology, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, Tokushima, 770-8503, Japan
  2. Department of Medical Pharmacology, Institute of Health Biosciences, The University of Tokushima Graduate School, 1-78-1, Shoumachi, Tokushima, 770-8505, Japan
  3. Department of Medicine and Bioregulatory Sciences, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, Tokushima, 770-8503, Japan
  4. Department of Clinical Pharmacy, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, Tokushima, 770-8503, Japan
  
• ISSN：1432-1912

文摘

Nifedipine is unstable under light and decomposes to a stable nitroso analog, nitrosonifedipine (NO-NIF). The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. However, the effects of NO-NIF on the pathogenesis related with oxidative stress, such as atherosclerosis and hypertension, are unclear. In this study, we investigated the effects of NO-NIF on angiotensin II (Ang II)-induced vascular remodeling. Ang II-induced thickening and fibrosis of aorta were inhibited by NO-NIF in mice. NO-NIF decreased reactive oxygen species (ROS) in the aorta and urinary 8-hydroxy-20-deoxyguanosine. Ang II-stimulated mRNA expressions of p22phox, CD68, F4/80, monocyte chemoattractant protein-1, and collagen I in the aorta were inhibited by NO-NIF. Moreover, NO-NIF inhibited Ang II-induced cell migration and proliferation of vascular smooth muscle cells (VSMCs). NO-NIF reduced Ang II-induced ROS to the control level detected by dihydroethidium staining and lucigenin chemiluminescence assay in VSMCs. NO-NIF suppressed phosphorylations of Akt and epidermal growth factor receptor induced by Ang II. However, NO-NIF had no effects on intracellular Ca2+ increase and protein kinase C-δ phosphorylation induced by Ang II in VSMCs. The electron paramagnetic resonance spectra indicated the continuous generation of NO-NIF radical of reaction with cultured VSMCs. These findings suggest that NO-NIF improves Ang II-induced vascular remodeling via the attenuation of oxidative stress.