Yamagishi Takahiro, Ishizuka Osamu, Imamura Tetsuya, Yokoyama Hitoshi, Ogawa Teruyuki, Kurizaki Yoshiki, Nishizawa Osamu, Andersson Karl-Erik
Department of Urology, Shinshu University School of Medicine, Matsumoto, Japan.
Neurourol Urodyn. 2015 Mar;34(3):280-5. doi: 10.1002/nau.22543. Epub 2013 Dec 23.
To determine if alpha1 -adrenergic receptors (AR) mediate bladder overactivity induced by cold stress in rats with bladder outlet obstruction (BOO).
The 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.
During 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.
Alpha1 -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.
确定α1 -肾上腺素能受体（AR）是否介导膀胱出口梗阻（BOO）大鼠冷应激诱导的膀胱过度活动。
结扎10周龄雌性Sprague-Dawley大鼠的尿道以造成BOO。4周后，在室温（RT，27±2°C）下进行20分钟的膀胱测压研究。然后给大鼠静脉注射0.3mg/kg萘哌地尔（n = 6）或赋形剂（n = 5）。5分钟后，将它们转移至低温（LT，4±2°C），并再次记录40分钟的膀胱测压模式。研究了BOO大鼠和假手术大鼠（n = 8）中α1A -和α1D -AR mRNA的表达水平以及降钙素基因相关肽（CGRP）阳性神经细胞上α1A -和α1D -AR免疫反应性的存在情况。
在LT暴露期间，接受赋形剂治疗的BOO大鼠表现出冷应激诱导的膀胱过度活动。与接受赋形剂治疗的动物相比，萘哌地尔治疗的大鼠中，LT诱导的基础压力增加以及排尿间隔和膀胱容量的减少均显著降低。在暴露于LT的BOO大鼠膀胱中，α1D -AR mRNA的表达明显高于假手术大鼠，并且CGRP阳性神经细胞上α1D -AR的免疫反应性趋于更明显。
α1 -AR介导BOO大鼠冷应激诱导的部分膀胱过度活动。冷应激增加了BOO大鼠中α1D -AR mRNA的表达以及CGRP阳性神经细胞上α1D -AR的免疫反应性。萘哌地尔部分抑制冷应激过度活动，表明其至少部分是通过α1D/1A -AR介导的。
