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Research ArticleArticle

Vasorelaxing Action of Rutaecarpine: Effects of Rutaecarpine on Calcium Channel Activities in Vascular Endothelial and Smooth Muscle Cells

Guei-Jane Wang, Xi-Chen Wu, Chieh-Fu Chen, Lie-Chwen Lin, Yi-Tsau Huang, Jie Shan and Peter K. T. Pang
Journal of Pharmacology and Experimental Therapeutics June 1999, 289 (3) 1237-1244;
Guei-Jane Wang
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Xi-Chen Wu
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Chieh-Fu Chen
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Lie-Chwen Lin
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Yi-Tsau Huang
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Jie Shan
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Peter K. T. Pang
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Abstract

Rutaecarpine (Rut) has been shown to induce hypotension and vasorelaxation. In vitro studies indicated that the vasorelaxant effect of Rut was largely endothelium-dependent. We previously reported that Rut increased intracellular Ca2+ concentrations ([Ca2+]i) in cultured rat endothelial cells (ECs) and decreased [Ca2+]i in cultured rat vascular smooth muscle (VSMCs) cells. The present results showed that the hypotensive effect of Rut (10–100 μg/kg i.v.) was significantly blocked by the nitric oxide synthase inhibitorNω-nitro-l-arginine. In aortic rings, Rut (0.1–3.0 μM)-induced vasorelaxation was inhibited byNω-nitro-l-arginine and hydroquinone but not by antagonists of the various K+ channels, 4-aminopyridine, apamin, charybdotoxin, or glibenclamide. Rut (0.1 and 1.0 μM) inhibited the norepinephrine-induced contraction generated by Ca2+ influx and at 1.0 μM increased cyclic GMP (cGMP) production in endothelium-intact rings and to a lesser extent in endothelium-denuded rings. In whole-cell patch-clamp recording, nonvoltage-dependent Ca2+ channels were recorded in ECs and Rut (0.1, 1.0 μM) elicited an opening of such channels. However, in VSMCs, Rut (10.0 μM) inhibited significantly the L-type voltage-dependent Ca2+ channels. In ECs cells, Rut (1.0, 10.0 μM) increased nitric oxide release in a Ca2+-dependent manner. Taken together, the results suggested that Rut lowered blood pressure by mainly activating the endothelial Ca2+-nitric oxide-cGMP pathway to reduce smooth muscle tone. Although the contribution seemed to be minor in nature, inhibition of contractile response in VSMCs, as evidenced by inhibition of Ca2+ currents, was also involved. Potassium channels, on the other hand, had no apparent roles.

Footnotes

  • Send reprint requests to: Prof. Chieh-Fu Chen, National Research Institute of Chinese Medicine, No. 155-1, Section 2, Li-Nong Street, Pei-tou District (112), Taipei, Taiwan, Republic of China. E-mail: jennyw{at}cma23.nricm.edu.tw

  • ↵1 This work was supported by Grants NSC87-2314-B077-001 from the National Science Council of the Republic of China (to C.F.C.).

  • Abbreviations:
    Rut
    rutaecarpine
    EC
    endothelial cell
    VSMC
    vascular smooth muscle cell
    NO
    nitric oxide
    l-NNA
    Nω-nitro-l-arginine
    NE
    norepinephrine
    VDCC
    voltage-dependent Ca2+ channel
    KCa
    Ca2+-dependent K+
    Kv
    voltage-dependent K+
    MAP
    mean arterial pressure
    FCS
    fetal calf serum
    HBSS
    Hanks’ balanced salt solution
    ROCC
    receptor-operated Ca2+ channel
    I-V
    current voltage
    • Received June 29, 1998.
    • Accepted January 28, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 289 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 289, Issue 3
1 Jun 1999
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Research ArticleArticle

Vasorelaxing Action of Rutaecarpine: Effects of Rutaecarpine on Calcium Channel Activities in Vascular Endothelial and Smooth Muscle Cells

Guei-Jane Wang, Xi-Chen Wu, Chieh-Fu Chen, Lie-Chwen Lin, Yi-Tsau Huang, Jie Shan and Peter K. T. Pang
Journal of Pharmacology and Experimental Therapeutics June 1, 1999, 289 (3) 1237-1244;

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Research ArticleArticle

Vasorelaxing Action of Rutaecarpine: Effects of Rutaecarpine on Calcium Channel Activities in Vascular Endothelial and Smooth Muscle Cells

Guei-Jane Wang, Xi-Chen Wu, Chieh-Fu Chen, Lie-Chwen Lin, Yi-Tsau Huang, Jie Shan and Peter K. T. Pang
Journal of Pharmacology and Experimental Therapeutics June 1, 1999, 289 (3) 1237-1244;
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