Kachur J F, Allbee W, Danho W, Gaginella T S
Regul Pept. 1987 Feb;17(2):63-9. doi: 10.1016/0167-0115(87)90013-9.
It is well established that bradykinin can stimulate mucosal electrolyte transport. However, the receptor type which mediates this effect has not been fully characterized. Recent studies have suggested that bradykinin and related kinins may act at two types of receptors designated as B1 and B2. We have determined the effect of bradykinin on electrolyte secretion across guinea pig ileal mucosa and longitudinal muscle in vitro in the presence and absence of D-Phe7-bradykinin (B2 antagonist) and des-Arg9-(Leu8)-bradykinin (B1 antagonist). The B2 antagonist (less than 100 microM) did not affect resting muscle tension or basal electrolyte transport but at 6-30 microM it caused a parallel rightward shift in the concentration-response curves to bradykinin in the mucosa (Ki = 4 microM) and muscle (Ki = 6 microM). Changes in electrolyte transport and muscle contractility evoked by bethanechol and substance P were not affected by the B2 antagonist (30 microM) in either the muscle or the mucosa. Moreover, changes in electrolyte transport and muscle contractility produced by bradykinin were not altered by the B1 antagonist (30 microM). Finally, the B1 agonist des-Arg9-bradykinin (10 nM-1 microM) was not active in either preparation. These data suggest that under normal conditions, ileal secretion and smooth muscle contractility in the guinea pig are regulated by B2-type bradykinin receptors.
缓激肽能刺激黏膜电解质转运，这一点已得到充分证实。然而，介导这种效应的受体类型尚未完全明确。最近的研究表明，缓激肽及相关激肽可能作用于两种被命名为B1和B2的受体。我们已测定在存在和不存在D - 苯丙氨酸7 - 缓激肽（B2拮抗剂）和去精氨酸9 - （亮氨酸8） - 缓激肽（B1拮抗剂）的情况下，缓激肽对豚鼠回肠黏膜和纵行肌电解质分泌的影响。B2拮抗剂（小于100微摩尔）不影响静息肌张力或基础电解质转运，但在6 - 30微摩尔时，它使黏膜（Ki = 4微摩尔）和肌肉（Ki = 6微摩尔）中缓激肽浓度 - 反应曲线平行右移。在肌肉或黏膜中，氨甲酰甲胆碱和P物质引起的电解质转运和肌肉收缩性变化不受B2拮抗剂（30微摩尔）影响。此外，缓激肽引起的电解质转运和肌肉收缩性变化也不受B1拮抗剂（30微摩尔）改变。最后，B1激动剂去精氨酸9 - 缓激肽（10纳摩尔 - 1微摩尔）在两种标本中均无活性。这些数据表明，在正常情况下，豚鼠回肠分泌和平滑肌收缩性受B2型缓激肽受体调节。
