Institute for Veterinary Physiology and Biochemistry, Justus-Liebig-University Giessen, Giessen, Germany.
Neurogastroenterol Motil. 2013 Sep;25(9):e581-90. doi: 10.1111/nmo.12165. Epub 2013 Jun 7.
In rat duodenum, bradykinin induces a relaxation followed by a contraction. Different types of ion channels and receptors as well as non-muscle cells have been suggested to be involved in this response. As it is unclear whether these changes are observed also in rat large intestine and the mechanisms which might underlie this response, the effect of bradykinin on rat colonic motility was tested.
Isometric contractions were measured on full-thickness preparations or preparations, from which individual layers had been dissected. The expression of bradykinin receptors was analyzed by immunohistochemistry and RT-PCR. Isolated intestinal muscle cells were investigated with Ca(2+) -imaging techniques.
Bradykinin caused a biphasic contractile response (initial relaxation followed by contraction) in rat colon, which was resistant against tetrodotoxin. The kinin-induced relaxation was inhibited by tetrapentylammonium chloride, a blocker of Ca(2+) -activated K(+) channels. Des-arg(9) -bradykinin did not induce any effect on the native colon, although after 5 h in vitro preincubation, a contractile response was evoked by this B1 receptor agonist. The consecutive ablation of adherent layers of the intestinal wall strongly reduced the response to bradykinin in comparison with a control stimulus, i.e., carbachol, suggesting a contribution of non-muscle cells in the mediation of this response.
CONCLUSIONS & INFERENCES: Bradykinin induced a biphasic change in contractility in the rat colon. In the native intestine, only the B2 receptor is involved in this effect. Neighboring cell obviously sensitize the smooth muscle to the stimulation of these receptors.
在大鼠十二指肠中，缓激肽诱导松弛继而收缩。不同类型的离子通道和受体以及非肌肉细胞被认为参与了这一反应。由于尚不清楚这些变化是否也存在于大鼠大肠中，以及可能导致这种反应的机制，因此测试了缓激肽对大鼠结肠蠕动的影响。
在全层制剂或分离单个层的制剂上测量等长收缩。通过免疫组织化学和 RT-PCR 分析缓激肽受体的表达。使用 Ca(2+) 成像技术研究分离的肠肌细胞。
缓激肽引起大鼠结肠的双相收缩反应（初始松弛后收缩），对河豚毒素有抗性。缓激肽诱导的松弛被四戊基氯化铵抑制，四戊基氯化铵是一种 Ca(2+) 激活的 K(+) 通道阻滞剂。尽管在体外孵育 5 小时后，这种 B1 受体激动剂会引起收缩反应，但去精氨酸 9-缓激肽对天然结肠没有任何作用。随后对肠壁的粘附层进行连续消融，与对照刺激物（即卡巴胆碱）相比，强烈降低了对缓激肽的反应，表明非肌肉细胞在介导这种反应中起作用。
缓激肽引起大鼠结肠收缩力的双相变化。在天然肠中，只有 B2 受体参与了这种作用。相邻细胞明显使平滑肌对这些受体的刺激敏感。
