2008年8月
Localization of CCK-1 R in the omasum and role of CCK in the regulation of ornasal contractions in sheep
DOMESTIC ANIMAL ENDOCRINOLOGY
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- 巻
- 35
- 号
- 2
- 開始ページ
- 231
- 終了ページ
- 244
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.domaniend.2008.05.004
- 出版者・発行元
- ELSEVIER SCIENCE INC
The present study examined localization of cholecystokinin receptor (CCK-R) mRNA in the muscle layer of the ovine omasum and role of CCK-R type 1 (CCK-1R) in the regulation of muscle contraction of the omasum. We demonstrated that not only CCK-R type 2 (CCK-2R) mRNA but also CCK-1R mRNA is highly expressed in the muscle layer of the ovine omasum. Application of CCK-8 to muscle strips of the greater curvature of the ovine omasum at 1-100 nM induced tonic contraction in a concentration-dependent manner, and the contractile effect of CCK-8 was inhibited by both CCK-1R antagonist lorglumide (IC(50) 2.7 and 7.9 mu M in the longitudinal and circular muscle, respectively) and CCK-2R antagonist PD135,158 (IC(50) 51.4 mu M in the longitudinal muscle), indicating that not only CCK-2R but also CCK-1R is functionally expressed in the plasma membrane of smooth muscles in the omasum and mediates action of exogenous CCK. Contractile effect of intravenous infusion of CCK-8 (1-30 pmol/kg/min) on omasal contraction was also confirmed in the in vivo experiments using conscious sheep in the absence and presence of atropine infusion (14.4 nmol/kg/min), and showed that circulating CCK increases omasal electromyographic (EMG) activity at lower plasma concentration than that it inhibits ruminal contractions. Taking account of our previous results in the in vivo study using other CCK-1R antagonist, it is suggested that circulating CCK, even at normal range of plasma concentration, plays a physiological role as a regulator of omasal contractions in sheep and CCK-1R mediates the action of CCK. (c) 2008 Elsevier Inc. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.domaniend.2008.05.004
- ISSN : 0739-7240
- PubMed ID : 18638666
- Web of Science ID : WOS:000258091700012