Capsaicin-induced Relaxation in Rabbit Coronary Artery.

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  • YEON Dongsoo
    Department of Physiology, Yonsei University College of Medicine
  • KWON Seongchun
    Department of Physiology, Yonsei University College of Medicine
  • LEE Youngho
    Department of Physiology, Yonsei University College of Medicine
  • LEEM Joongwoo
    Department of Physiology, Yonsei University College of Medicine
  • NAM Taicksang
    Department of Physiology, Yonsei University College of Medicine
  • AHN Ducksun
    Department of Physiology, Yonsei University College of Medicine

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In the present study mechanism of inhibitory effects of capsaicin on the contractility of rabbit coronary artery were studied by measurement of isometric tension and intracellular Ca2+ concentration. Capsaicin (1 μM to 30 μM) relaxed the coronary artery pre-contracted with prostaglandin (PG) F2α (1 μM) in a concentration-dependent manner. The PGF2 α-induced increase in intracellular Ca2+ concentration was also inhibited. The effects of capsaicin were readily reversed by washing capsaicin from the bath. Capsaicin-induced relaxation was not attenuated by pretreatment with capsazepine (1 μM), a blocker of vanilloid receptor or ruthenium red (1 μM), a blocker of non-selective cation channel. Previous exposure to a high concentration of capsaicin (100 μM) or repeated application of capsaicin did not eliminate the relaxation response to subsequent application of capsaicin. Increasing the external K+ concentration to 80 mM significantly attenuated the capsaicin-induced relaxation with simultaneous change in intracellular Ca2+ concentration. Pretreatment with iberiotoxin (100 nM), a blocker of Ca2+-activated K+ channel, only partially inhibited the capsaicin-induced relaxation. However, application of 4-aminopyridine (4-AP, 1 mM), a blocker of delayed rectifier K+ current significantly inhibited the capsaicin-induced relaxation with concomitant attenuation of the effect on intracellular Ca2+ concentration. These results indicate that capsaicin may have a direct relaxing effect on the smooth muscle contractility, and relaxation may be due to activation of the 4-AP-sensitive, delayed rectifier K+ channels in the rabbit coronary artery.

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