Ohmura M, Kondo A, Saito M
Department of Urology, Nagoya University School of Medicine, Japan.
Urol Int. 1997;59(4):221-5. doi: 10.1159/000283067.
Tachykinins act as stimulants of the isolated urinary bladder. However, the efferent role of tachykinins on detrusor function is controversial. We investigated the contractility of isolated human neurogenic bladders taken from patients with myelomeningocele or sacral agenesis, and tested the response to neurokinin A (NKA), neuromedin K (NKB), and substance P (SP). The contractile strengths were compared with normal controls. All tachykinins investigated induced significant contractions in both neurogenic and control bladders. The rank order of contractile potency was the same in both groups, namely, NKA > NKB > SP. The contraction induced by SP was not affected by atropine, but was completely blocked by [Sar9,Met(O2)11]-SP (a SP antagonist). Responses to electrical field stimulation were not changed by the SP antagonist. The contractile magnitude to field stimulation was also not altered by administration of 10(-6) M tachykinins. Responses of the neurogenic bladder to NKA and SP were significantly greater than the control. There were no differences in the response to KCl administration between the 2 groups. We conclude that hypersensitivity to NKA and SP in neurogenic bladders may contribute to bladder dysfunction in patients with sacral cord lesions.
速激肽可作为离体膀胱的刺激物。然而，速激肽对逼尿肌功能的传出作用存在争议。我们研究了取自脊髓脊膜膨出或骶骨发育不全患者的离体人神经源性膀胱的收缩性，并测试了其对神经激肽A（NKA）、神经介素K（NKB）和P物质（SP）的反应。将收缩强度与正常对照进行比较。所有研究的速激肽在神经源性膀胱和对照膀胱中均诱导出显著收缩。两组的收缩效力排序相同，即NKA > NKB > SP。SP诱导的收缩不受阿托品影响，但被[Sar9,Met(O2)11]-SP（一种SP拮抗剂）完全阻断。电场刺激的反应不受SP拮抗剂影响。给予10(-6) M速激肽后，对电场刺激的收缩幅度也未改变。神经源性膀胱对NKA和SP的反应明显大于对照组。两组之间对氯化钾给药的反应没有差异。我们得出结论，神经源性膀胱对NKA和SP的超敏反应可能导致骶髓损伤患者的膀胱功能障碍。
