Maggi C A, Giuliani S, Santicioli P, Abelli L, Giachetti A
Pharmacology Department, A. Menarini Pharmaceuticals, Florence and Menarini Sud, Rome, Italy.
J Urol. 1991 Jan;145(1):184-7. doi: 10.1016/s0022-5347(17)38287-3.
We have determined the ability of [beta Ala8]-NKA(4-10), a selective agonist for NK-2 tachykinin receptors to stimulate micturition in anesthetized rats and guinea-pigs. In both species, the intravesical instillation of the peptide at microM concentrations reduced bladder capacity and residual volume, indicating a facilitatory effect on reflex micturition. At these concentrations, no plasma extravasation was produced as determined by the Evans blue content of the organ. In experiments on the isolated rat or guinea-pig bladder strips, the NK-2 receptor agonist induced powerful contractions. In a in vitro model of the guinea-pig whole bladder the intravesical instillation of the NK-2 agonist facilitated the occurrence of rhythmic contractile activity. It is concluded from these studies that intravenous administration of [beta Ala8]-NKA(4-10) exerts a facilitatory effect on the micturition reflex, presumably involving the ability of the NK-2 receptor agonist to cross the urothelium and stimulate smooth muscle contraction.
我们已经测定了[β-丙氨酸8]-NKA(4-10)（一种NK-2速激肽受体的选择性激动剂）刺激麻醉大鼠和豚鼠排尿的能力。在这两个物种中，膀胱内灌注微摩尔浓度的该肽可降低膀胱容量和残余尿量，表明对反射性排尿有促进作用。在这些浓度下，通过器官的伊文思蓝含量测定未产生血浆外渗。在对分离的大鼠或豚鼠膀胱条的实验中，NK-2受体激动剂可诱导强烈收缩。在豚鼠全膀胱的体外模型中，膀胱内灌注NK-2激动剂促进了节律性收缩活动的发生。从这些研究得出结论，静脉注射[β-丙氨酸8]-NKA(4-10)对排尿反射有促进作用，推测这涉及NK-2受体激动剂穿过尿路上皮并刺激平滑肌收缩的能力。
