학술논문
A Novel Pathway Underlying the Inhibitory Effects of Melatonin on Isolated Rat Urinary Bladder Contraction
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- 영문명
- A Novel Pathway Underlying the Inhibitory Effects of Melatonin on Isolated Rat Urinary Bladder Contraction
- 발행기관
- 대한생리학회-대한약리학회
- 저자명
- June Hyun Han In Ho Chang Soon Chul Myung Moo Yeol Lee Won Yong Kim Seo Yeon Lee Shin Young Lee Seun
- 간행물 정보
- 『The Korean Journal of Physiology & Pharmacology』제16권 제1호, 37~42쪽, 전체 6쪽
- 주제분류
- 의약학 > 의학일반
- 파일형태
- 발행일자
- 2012.01.01
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국문 초록
영문 초록
The aim of the present study was to elucidate the direct effects of melatonin on bladder activity and to determine the mechanisms responsible for the detrusor activity of melatonin in the isolated rat bladder. We evaluated the effects of melatonin on the contractions induced by phenylephrine (PE), acetylcholine (ACh), bethanechol (BCh), KCl, and electrical field stimulation (EFS) in 20 detrusor smooth muscle samples from Sprague-Dawley rats. To determine the mechanisms underlying the inhibitory responses to melatonin, melatonin-pretreated muscle strips were exposed to a calcium channel antagonist (verapamil), three potassium channel blockers [tetraethyl ammonium (TEA), 4-aminopyridine (4-AP), and glibenclamide], a direct voltage-dependent calcium channel opener (Bay K 8644), and a specific calcium/calmodulin-dependent kinase II (CaMKII) inhibitor (KN-93). Melatonin pretreatment (10－8∼10－6 M) decreased the contractile responses induced by PE (10－9∼10－4 M) and Ach (10－9∼10－4 M) in a dose-dependent manner. Melatonin (10－7 M) also blocked contraction induced by high KCl ([KCl]ECF; 35 mM, 70 mM, 105 mM, and 140 mM) and EFS. Melatonin (10－7 M) potentiated the relaxation response of the strips by verapamil, but other potassium channel blockers did not change melatonin activity. Melatonin pretreatment significantly decreased contractile responses induced by Bay K 8644 (10－11∼10－7 M). KN-93 enhanced melatonin-induced relaxation. The present results suggest that melatonin can inhibit bladder smooth muscle contraction through a voltage-dependent, calcium-antagonistic mechanism and through the inhibition of the calmodulin/CaMKII system.
목차
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