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Article

Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro

  • Authors:
    • Chih-Cheng Lu
    • Hsien-Hui Chung
    • Juei-Tang Cheng
  • View Affiliations / Copyright

    Affiliations: Department of Surgery, Chi-Mei Medical Center, Liou-Ying, Tainan, Taiwan, R.O.C., Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, R.O.C., Department of Medical Research, Chi-Mei Medical Center, Yong Kang, Tainan, Taiwan, R.O.C.
  • Pages: 281-285
    |
    Published online on: January 20, 2011
       https://doi.org/10.3892/etm.2011.201
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Abstract

The merit of opioid µ-receptor activation in the improvement of benign prostatic hyperplasia (BPH) remains obscure. In the present study, we used loperamide to identify the subtype of opioid µ-receptors involved in prostatic relaxation and investigate the possible mechanism of this relaxation. Prostate strips were isolated from 12-week-old male Wistar rats for identification of isometric tension. The prostate strips were precontracted with either 1 µmol/l phenylephrine or 50 mmol/l KCl. The decrease in muscle tone (relaxation) was then characterized after cumulative administration of loperamide (0.1 to 10 µmol/l) into the organ bath for the concentration-dependent study. Pretreatment with specific blockers or antagonists was carried out to compare the changes in loperamide-induced relaxation. Loperamide produced a marked relaxation in the isolated prostates precontracted with phenylephrine or KCl in a dose-dependent manner. This relaxation was abolished by cyprodime, a selective opioid µ-receptor antagonist, but was not modified by naloxonazine at a dose sufficient to block the opioid µ-1 receptors. Treatment with an agonist for opioid µ-1 receptors also failed to modify the muscle tone. Moreover, the relaxation by loperamide was attenuated by glibenclamide at a dose sufficient to block ATP-sensitive K+ channels. In addition, this action of loperamide was abolished by protein kinase A (PKA) inhibitor and enhanced by the inhibitor of phosphodiesterase for cyclic AMP (cAMP). Our results suggest that loperamide induces prostatic relaxation through activation of opioid µ-2 receptors via the cAMP-PKA pathway to open ATP-sensitive K+ channels.
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Copy and paste a formatted citation
Spandidos Publications style
Lu C, Chung H and Cheng J: Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro. Exp Ther Med 2: 281-285, 2011.
APA
Lu, C., Chung, H., & Cheng, J. (2011). Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro. Experimental and Therapeutic Medicine, 2, 281-285. https://doi.org/10.3892/etm.2011.201
MLA
Lu, C., Chung, H., Cheng, J."Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro". Experimental and Therapeutic Medicine 2.2 (2011): 281-285.
Chicago
Lu, C., Chung, H., Cheng, J."Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro". Experimental and Therapeutic Medicine 2, no. 2 (2011): 281-285. https://doi.org/10.3892/etm.2011.201
Copy and paste a formatted citation
x
Spandidos Publications style
Lu C, Chung H and Cheng J: Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro. Exp Ther Med 2: 281-285, 2011.
APA
Lu, C., Chung, H., & Cheng, J. (2011). Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro. Experimental and Therapeutic Medicine, 2, 281-285. https://doi.org/10.3892/etm.2011.201
MLA
Lu, C., Chung, H., Cheng, J."Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro". Experimental and Therapeutic Medicine 2.2 (2011): 281-285.
Chicago
Lu, C., Chung, H., Cheng, J."Prostatic relaxation induced by loperamide is mediated through activation of opioid µ-2 receptors in vitro". Experimental and Therapeutic Medicine 2, no. 2 (2011): 281-285. https://doi.org/10.3892/etm.2011.201
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