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Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels

  • Authors:
    • Guanying Hu
    • Xixiong Li
    • Sanyin Zhang
    • Xin Wang
  • View Affiliations / Copyright

    Affiliations: Basic Medical College, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China
    Copyright: © Hu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 27-34
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    Published online on: May 18, 2016
       https://doi.org/10.3892/br.2016.680
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Abstract

The aim of the present study was to elucidate the roles of endothelium-derived hyperpolarizing factors (EDHFs) and nitric oxide (NO) in mediating the vasodilatation response to astragaloside IV and the effects of astragaloside IV on voltage‑dependent Ca2+ channels and receptor‑operated Ca2+ channels in rat thoracic aortic rings precontracted with potassium chloride (KCl; 60 mM) or phenylephrine (PHE; 1 µM). The results showed that astragaloside IV (1x10‑4‑3x10‑1 g/l) concentration‑dependently relaxed the contraction induced by KCl (10‑90 mM) or PHE (1x10‑9‑3x10‑5 µM) and inhibited concentration‑contraction curves for the two vasoconstrictors in the aortic rings. Preincubation with Nω‑nitro‑L‑arginine methyl ester (L‑NAME, 100 µM) significantly attenuated astragaloside IV‑induced relaxation in the endothelium‑intact and ‑denuded arterial rings precontracted with PHE. Astragaloside IV, following preincubation with L‑NAME (100 µM) plus indomethacin (10 µM), exerted vasodilatation, which was depressed by tetraethtylamine (1 mM) and propargylglycine (100 µM), but not by carbenoxolone (10 µM), catalase (500 U/ml) or proadifen hydrochloride (10 µM). The action mode of astragaloside IV was evident in comparison to nifedipine. Inhibition of PHE‑induced contraction by astragaloside IV (100 mg/l) was more potent compared to inhibition of KCl‑induced contraction, while inhibition of KCl‑induced contraction by nifedipine (100 mg/l) was more potent compared to inhibition of PHE‑induced contraction by nifedipine (100 mg/l). In addition, the combination of astragaloside IV and nifedipine exhibited synergistic and additive inhibitory effects on contraction evoked by KCl, which was similar to PHE. In conclusion, astragaloside IV, as a Ca2+ antagonist, relaxes the vessels through the blockade of superior receptor‑operated Ca2+ and inferior voltage‑dependent Ca2+ channels, which modulate NO from vascular endothelial cells and vascular smooth muscle cells, and EDHFs including K+ and hydrogen sulfide.
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Copy and paste a formatted citation
Spandidos Publications style
Hu G, Li X, Zhang S and Wang X: Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels. Biomed Rep 5: 27-34, 2016.
APA
Hu, G., Li, X., Zhang, S., & Wang, X. (2016). Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels. Biomedical Reports, 5, 27-34. https://doi.org/10.3892/br.2016.680
MLA
Hu, G., Li, X., Zhang, S., Wang, X."Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels". Biomedical Reports 5.1 (2016): 27-34.
Chicago
Hu, G., Li, X., Zhang, S., Wang, X."Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels". Biomedical Reports 5, no. 1 (2016): 27-34. https://doi.org/10.3892/br.2016.680
Copy and paste a formatted citation
x
Spandidos Publications style
Hu G, Li X, Zhang S and Wang X: Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels. Biomed Rep 5: 27-34, 2016.
APA
Hu, G., Li, X., Zhang, S., & Wang, X. (2016). Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels. Biomedical Reports, 5, 27-34. https://doi.org/10.3892/br.2016.680
MLA
Hu, G., Li, X., Zhang, S., Wang, X."Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels". Biomedical Reports 5.1 (2016): 27-34.
Chicago
Hu, G., Li, X., Zhang, S., Wang, X."Association of rat thoracic aorta dilatation by astragaloside IV with the generation of endothelium‑derived hyperpolarizing factors and nitric oxide, and the blockade of Ca2+ channels". Biomedical Reports 5, no. 1 (2016): 27-34. https://doi.org/10.3892/br.2016.680
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