Dopaminergic urethral closure mechanisms in a rat model of Parkinson's disease.
Dopaminergic urethral closure mechanisms in a rat model of Parkinson's disease.
复制标题
帕金森病大鼠模型中的多巴胺能尿道闭合机制。
DOI：
10.1002/nau.23989
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Shinohara N.
中科院分区：
文献类型：
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作者：
Ouchi M;Kitta T;Kanno Y;Higuchi M;Togo M;Takahashi Y;Moriya K;Shinohara N.
目的尿失禁在帕金森病 (PD) 患者中很常见。在本研究中，我们研究了黑质致密部注射6-羟基多巴胺诱导的PD大鼠模型的尿道功能，以及多巴胺D1和D2样受体的选择性激动剂/拮抗剂在主动尿道闭合机制中的作用。结果：与对照组相比，未经治疗的 PD 大鼠组的平均渗漏点压力和平均主动尿道反应值显着较小。在PD模型中，多巴胺D1样受体激动剂治疗后尿道主动反应显着增加，而多巴胺D2样受体激动剂诱导的主动尿道反应显着下降。 PD 大鼠对 D2 样受体激动剂的反应被多巴胺 D2 样受体拮抗剂抑制。结论我们的结果表明，当多巴胺耗尽时，主动尿道闭合机制显着受损。在PD大鼠中，中枢神经系统上的多巴胺D1样受体活性似乎部分补偿了因缺乏多巴胺而受到的尿道功能的负面影响，而多巴胺D2样受体活性可能会加剧尿漏，因为这种激活的受体在腹内压升高时对尿道压力产生负面影响。
AimsUrinary incontinence is prevalent among patients with Parkinson's disease (PD). In the present study, we investigated urethral functions in a rat model of PD induced by 6‐hydroxydopamine injection at their substantia nigra pars compacta as well as the roles of selective agonists/antagonist of dopamine D1‐ and D2‐like receptors in active urethral closure mechanisms.MethodsWe measured changes in the urethral pressure amplitude during electrical stimulation, urethral baseline pressure, and leak point pressure after intravenous administration of selective agonists or antagonists of the dopamine D1‐ and D2‐like receptors in a rat model of PD.ResultsThe mean leak point pressure and the mean active urethral response values were significantly smaller for the untreated PD rat group compared with the control group. In PD model, the active urethral response increased significantly after treatment with the dopamine D1‐like receptor agonist, whereas that induced by the dopamine D2‐like receptor agonist decreased significantly. The response to the D2‐like receptor agonist was suppressed in the PD rat by the dopamine D2‐like receptor antagonist.ConclusionOur results suggest that the active urethral closure mechanisms are significantly impaired when dopamine is depleted. In the PD rat, dopamine D1‐like receptor activity on the central nervous system appear to partially compensate for urethral functions negatively impacted by the lack of dopamine, whereas dopamine D2‐like receptor activity might exacerbate urinary leakage owing to the negative effect of this activated receptor on urethral pressure under increased intra‐abdominal pressure.