Inhibition by Clonidine of the Carbachol-Induced Tension Development and Nonselective Cationic Current in Guinea Pig Ileal Myocytes.

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  • Chung SeungSoo
    Department of Physiology, College of Medicine, Yonsei University
  • Kwon SeongChun
    Department of Physiology, College of Medicine, Yonsei University
  • Kim YunSuk
    Department of Physiology, College of Medicine, Yonsei University
  • Ahn DuckSun
    Department of Physiology, College of Medicine, Yonsei University
  • Lee YoungHo
    Department of Physiology, College of Medicine, Yonsei University
  • Nam TaickSang
    Department of Physiology, College of Medicine, Yonsei University

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Abstract

Effects of clonidine, an imidazoline derivative as well as α2-adrenoceptor agonist, on carbachol (CCh)-evoked contraction in guinea pig ileal smooth muscle were studied using isometric tension recording. To investigate the cellular mechanisms of the inhibitory effect of clonidine, its effects on CCh-evoked nonselective cationic current (ICCh), voltage-dependent Ca2+ current (ICa) and voltage-dependent K+ current (IK) was also studied using patch-clamp recording techniques in single ileal cells. Clonidine inhibited the contraction evoked by CCh (1 μM) in a concentration-dependent manner with an IC50 valve of 61.7 ± 2.5 μM. High K+ (40 mM)-evoked contraction was only slightly inhibited even when clonidine was used at 300 μM. Externally applied clonidine inhibited ICCh dose-dependently with an IC50 of 42.0 ± 2.6 μM. When applied internally via patch pipettes, clonidine was without effect. An ICCh-like current induced by GTPγS was also inhibited by bath application of clonidine. None of KU14R and BU224, both imidazoline receptor blockers, and yohimbine, an α2-adrenergic blocker, significantly affects the inhibitory effect of clonidine on ICCh. Clonidine (300 μM) only slightly decreased membrane currents flowing through voltage-gated Ca2+ channels or K+ channels. These data indicate that clonidine relaxes smooth muscle contraction produced by muscarinic receptor activation and suggest that the effect of clonidine seems due mainly to inhibition of ICCh via acting directly on the involved cationic channel.

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