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首页> 外文期刊>The journal of sexual medicine >Phosphodiesterase type 5 expression in human and rat lower urinary tract tissues and the effect of tadalafil on prostate gland oxygenation in spontaneously hypertensive rats.
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Phosphodiesterase type 5 expression in human and rat lower urinary tract tissues and the effect of tadalafil on prostate gland oxygenation in spontaneously hypertensive rats.

机译：人和大鼠下尿道组织中磷酸二酯酶5型的表达以及他达拉非对自发性高血压大鼠前列腺氧化的影响。

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INTRODUCTION: In humans, prostate phosphodiesterase type 5 inhibitors (PDE5) expression was prominently localized in the endothelial and smooth muscle cells of the vascular bed, suggesting a possible action of PDE5 inhibitors (PDE5i) on prostate blood flow. AIM: To investigate PDE5 expression in human and rat lower urinary tract (LUT) tissues, including vasculature, and determine the effects of PDE5 inhibition with tadalafil on prostatic blood perfusion. MAIN OUTCOME MEASURES: Human vesicular-deferential arteries (which originate from the inferior vesical artery, the main arterial source of blood supply to the bladder and prostate) were analyzed for PDE5 expression and activity. The effects of tadalafil on prostate oxygenation were studied in spontaneously hypertensive rats (SHR), characterized by ischemia/hypoxia of the genitourinary tract. METHODS: PDE5 expression was evaluated by quantitative reverse transcription-polymerase chain reaction and immunohistochemistry. SHR were treated with tadalafil (2 mg/kg/day) for 1, 7, or 28 days and compared with untreated SHR and the unaffected counterpart Wistar-Kyoto (WKY) rats. Prostate oxygenation was detected by Hypoxyprobe-1 and hypoxia markers (hypoxia-inducible factor-1alpha[HIF-1alpha] and endothelin-1 type B [ETB]) immunostaining. RESULTS: Human vesicular-deferential artery expressed high levels of PDE5, similar to corpora cavernosa, immunolocalized in the endothelial and smooth muscle layer. In these arteries, tadalafil inhibited cyclic guanosine monophosphate breakdown (half maximal inhibitory concentration (IC(50) ) in the low nanomolar range, as in corpora cavernosa) and increased the relaxant response to sodium nitroprusside. SHR prostate resulted markedly hypoxic (hypoxyprobe immunopositivity) and positive for HIF-1alpha and ETB, while tadalafil treatment restored oxygenation to WKY level at each time point. The mRNA expression of the HIF-1alpha target gene, BCL2/adenovirus E1B 19 kDa interacting protein 3, was significantly increased in SHR prostate and partially restored to WKY level by tadalafil. CONCLUSION: Human vesicular-deferential artery is characterized by a high expression and activity of PDE5, which was inhibited by tadalafil in vitro. In SHR, tadalafil increases prostate tissue oxygenation, thus suggesting a possible mechanism through which PDE5i exert beneficial effects on LUT symptoms.
机译：简介：在人类中，前列腺磷酸二酯酶5型抑制剂（PDE5）的表达明显位于血管床的内皮细胞和平滑肌细胞中，提示PDE5抑制剂（PDE5i）对前列腺血流的可能作用。目的：研究PDE5在人和大鼠下尿道（LUT）组织（包括脉管系统）中的表达，并测定他达拉非对PDE5的抑制作用对前列腺血液灌注的影响。主要观察指标：分析人水泡防御性动脉（起源于下膀胱动脉，膀胱和前列腺的主要动脉血供来源）的PDE5表达和活性。在以高血压和泌尿生殖道缺氧为特征的自发性高血压大鼠（SHR）中研究了他达拉非对前列腺氧合的影响。方法：采用定量逆转录聚合酶链反应和免疫组化方法检测PDE5的表达。用他达拉非（2 mg / kg /天）治疗SHR 1、7或28天，并与未治疗的SHR和未患病的Wistar-Kyoto（WKY）大鼠进行比较。通过Hypoxyprobe-1和低氧标记物（低氧诱导因子-1α[HIF-1α]和内皮素-1 B型[ETB]）免疫染色检测前列腺氧合。结果：人水泡防御动脉高表达PDE5，类似于海绵体，免疫定位在内皮和平滑肌层。在这些动脉中，他达拉非抑制环状鸟苷单磷酸的分解（如在海绵体中一样，在低纳摩尔范围内的半数最大抑制浓度（IC（50）））并增加了对硝普钠的松弛反应。 SHR前列腺明显缺氧（hypooxyprobe免疫阳性），HIF-1α和ETB阳性，而他达拉非治疗在每个时间点均将氧合恢复到WKY水平。 HIF-1alpha靶基因BCL2 /腺病毒E1B 19 kDa相互作用蛋白3的mRNA表达在SHR前列腺中显着增加，并通过他达拉非部分恢复至WKY水平。结论：人水泡防御动脉的特点是PDE5的高表达和活性，其在体外被他达拉非抑制。在SHR中，他达拉非可增加前列腺组织的氧合作用，从而提示PDE5i对LUT症状产生有益作用的可能机制。

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