Mattiasson A, Andersson K E, Sjögren C
J Urol. 1985 Feb;133(2):298-303. doi: 10.1016/s0022-5347(17)48927-0.
Isolated urethral muscle from rabbit and man was subjected to electrical field stimulation and the components of the resulting contraction were analyzed. Contraction usually consisted of 2 main components. One was rapidly developing, non-adrenergic and atropine-resistant. The other developed more slowly and was sensitive to alpha-adrenoceptor blockade and to chemical sympathectomy with 6-hydroxydopamine. By lowering the temperature from 37C to 20C, these contraction components could be separated from each other. Both could be blocked by tetrodotoxin but the effects of this drug were not consistent in human tissue. Characteristic for the initial contraction component was its dependence on the tension of the preparation; it increased with increasing tension. The adrenergic part of the contraction could be effectively blocked by phentolamine and prazosin, whereas rauwolscine was less effective. Atropine and scopolamine also inhibited the adrenergic part of the contraction, whereas acetylcholine caused a transient increase. The non-adrenergic contraction component was less sensitive to deprivation of extracellular Ca2+ than the adrenergic; almost 40 per cent remained after exposure to Ca2+ free solution for 40 min., whereas the adrenergic component disappeared after 20 min. exposure. Light and electron microscopic investigation revealed 3 distinct layers of the rabbit urethral wall, 1 outer consisting of smooth and striated muscle, 1 middle consisting of smooth muscle only, and a submucosal layer where vessels and smooth muscle cells were found. Removal of the longitudinal muscle layer did not change the responses to electrical stimulation. The results suggest that the electrically induced adrenergic activation of urethral muscle of both rabbit and man was mediated mainly via alpha-adrenoceptors and that this muscle is innervated not only by sympathetic, adrenergic nerves but also by a type of nerve able to release a non-cholinergic, contraction-mediating transmitter.
对兔和人的离体尿道肌肉施加电场刺激,并对由此产生的收缩成分进行分析。收缩通常由两个主要成分组成。一个是快速发展的、非肾上腺素能且对阿托品耐药的。另一个发展较慢,对α-肾上腺素能受体阻断和用6-羟基多巴胺进行化学交感神经切除术敏感。通过将温度从37℃降至20℃,这些收缩成分可以彼此分离。两者都可被河豚毒素阻断,但该药物在人体组织中的作用并不一致。初始收缩成分的特点是其依赖于标本的张力;它随张力增加而增加。收缩的肾上腺素能部分可被酚妥拉明和哌唑嗪有效阻断,而育亨宾的效果较差。阿托品和东莨菪碱也抑制收缩的肾上腺素能部分,而乙酰胆碱则引起短暂增加。非肾上腺素能收缩成分对细胞外Ca2+剥夺的敏感性低于肾上腺素能成分;在无Ca2+溶液中暴露40分钟后,近40%的成分仍保留,而肾上腺素能成分在暴露20分钟后消失。光镜和电镜研究显示兔尿道壁有3个不同的层,1个外层由平滑肌和横纹肌组成,1个中层仅由平滑肌组成,还有1个黏膜下层,其中有血管和平滑肌细胞。去除纵肌层并不改变对电刺激的反应。结果表明,兔和人尿道肌肉的电诱导肾上腺素能激活主要通过α-肾上腺素能受体介导,并且该肌肉不仅由交感肾上腺素能神经支配,还由一种能够释放非胆碱能收缩介导递质的神经支配。