Alpha1-adrenergic receptors mediate detrusor overactivity induced by cold stress in rats with bladder outlet obstruction
Alpha1-adrenergic receptors mediate detrusor overactivity induced by cold stress in rats with bladder outlet obstruction
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α1-肾上腺素能受体介导膀胱出口梗阻大鼠冷应激诱导的逼尿肌过度活动
DOI：
10.1002/nau.22543
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发表时间：
2014
期刊：
影响因子：
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通讯作者：
Andersson KE
中科院分区：
文献类型：
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作者：
Yamagishi T;Ishizuka O;Imamura T;Yokoyama H;Ogawa T;Kurizaki Y;Nishizawa O;Andersson KE
目的确定是否α 1-肾上腺素能受体（AR）介导膀胱出口梗阻（BOO）大鼠中由冷应激诱导的膀胱过度活动。材料和方法将10周龄雌性道利大鼠的尿道结扎以产生BOO。4周后，在室温（RT，27 ± 2°C）下进行膀胱测压研究20分钟。然后对大鼠静脉注射0.3 mg/kg萘哌地尔（n = 6）或溶剂（n = 5）。5分钟后，将它们转移到低温（LT，4 ± 2°C），并再次记录膀胱测压模式40分钟。在BOO大鼠和假手术大鼠（n = 8）的表达水平的α 1A-和α 1D-AR mRNA和降钙素基因相关肽（CGRP）阳性神经细胞上的α 1A-和α 1D-AR免疫反应性的存在进行了调查。在萘哌地尔给药大鼠中，与溶剂给药动物相比，LT诱导的基础压升高以及排尿间期和膀胱容量降低均显著降低。在低温暴露的BOO大鼠膀胱中，alpha 1 D-AR mRNA的表达显著高于假手术组，且CGRP阳性神经细胞上的alpha 1 D-AR的免疫反应性更明显。结论alpha 1-AR介导了BOO大鼠冷应激引起的部分膀胱过度活动。冷应激增加BOO大鼠CGRP阳性神经细胞上的alpha 1D-AR mRNA表达和alpha 1D-AR的免疫反应性。萘哌地尔部分抑制冷应激过度活动，表明其至少部分通过α 1D/1A-ARs. Neurourol介导。Urodynam。34：280-285，2015.© 2013 Wiley Periodicals，Inc.
PurposeTo determine if alpha1‐adrenergic receptors (AR) mediate bladder overactivity induced by cold stress in rats with bladder outlet obstruction (BOO).Materials and MethodsThe urethras of 10‐week‐old female Sprague‐Dawley rats were ligated to create BOO. After 4 weeks, cystometric investigations were performed at room temperature (RT, 27 ± 2°C) for 20 min. The rats were then given 0.3 mg/kg naftopidil (n = 6) or vehicle (n = 5) intravenously. Five minutes later, they were transferred to low temperature (LT, 4 ± 2°C), and the cystometric patterns were again recorded for 40 min. In BOO rats and in sham‐operated rats (n = 8) the expression levels of alpha1A‐ and alpha1D‐AR mRNAs and the presence of alpha1A‐ and alpha1D‐AR immunoreactivity on calcitonin gene‐related peptide (CGRP)‐positive nerve cells were investigated.ResultsDuring LT exposure, the vehicle‐treated BOO rats exhibited cold stress‐induced bladder overactivity. In the naftopidil‐treated rats, the increase of basal pressure and decreases of both voiding interval and bladder capacity induced by LT were significantly reduced compared to the vehicle‐treated animals. In the bladders of BOO rats exposed to LT, the expression of alpha1D‐AR mRNA was significantly higher than in sham‐operated rats, and the immunoreactivity for alpha1D‐ARs on the CGRP‐positive nerve cells tended to be more pronounced.ConclusionsAlpha1‐ARs mediate part of the bladder overactivity induced by cold stress in rats with BOO. Cold stress increases the expression of alpha1D‐AR mRNA and the immunoreactivity for alpha1D‐ARs on the CGRP‐positive nerve cells in BOO rats. Naftopidil partially inhibits the cold stress overactivity, suggesting that it is mediated, at least partially, through alpha1D/1A‐ARs.Neurourol. Urodynam. 34:280–285, 2015. © 2013 Wiley Periodicals, Inc.