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Impact of hypertension, aging, and antihypertensive treatment on the morphology of the pudendal artery.

机译:高血压,衰老和降压治疗对阴部动脉形态的影响。

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INTRODUCTION: Aging and hypertension increase the risk of erectile dysfunction (ED) and cardiovascular disease. Arterial insufficiency is likely a primary factor in hypertension-related ED. Given the dominance of internal pudendal arteries in controlling penile vascular resistance, pathological changes in this vessel would be critical for inducing ED in aged hypertensives. AIM: We assessed the age-related impact of hypertension and its treatment on erectile function and pudendal artery structure in young and old spontaneously hypertensive rats (SHRs). METHODS: Erectile responses were monitored in 15- and 77-week-old SHR and Wistar Kyoto (WKY) rats using apomorphine (80 mg/kg). At sacrifice, the vasculature was perfusion-fixed and aorta, renal, mesenteric, and internal pudendal arteries assessed morphometrically using light and electron microscopy. A separate group of 15-week SHR were treated with enalapril and hydrochlorothiazide (30 mg/kg/day, 2 weeks) followed by 2 weeks off treatment, after which the same vessels were assessed morphometrically. Arterial pressures were determined using radiotelemetry. MAIN OUTCOMES MEASURED: Erectile function, vessel morphology (lumen diameter, wall thickness, cross-sectional area, extracellular matrix [ECM]) and arterial pressure. RESULTS: Erectile responses were similar in young SHR and WKY (1.7 +/- 0.80 vs. 1.4 +/- 0.85) but declined significantly in aged SHR (0.3 +/- 0.49). Vascular aging in SHR was associated with striking pudendal remodeling, characterized by marked neointimal proliferation and disruptions of the internal elastic lamina. This remodeling involved thickening of the medial layer (35 +/- 6.0 microm vs. 81 +/- 3.5 microm, P < 0.01), decreased lumen diameter (282 +/- 6.3 microm vs. 250 +/- 12.4 microm, P < 0.05) and increased ECM (10 +/- 2.0 microm(2) vs. 26 +/- 10.6 microm(2), P < 0.001). In old pudendals, there were significantly more round synthetic smooth muscle cells bordering the intima and in the neointima. Antihypertensive treatment decreased the wall:lumen ratio in young SHR pudendal arteries (-17%). CONCLUSIONS: Vascular aging in SHR with ED involved distinctive pathogenic remodeling in the internal pudendal artery. In young SHR, brief antihypertensive therapy was able to regress this abnormal morphology.
机译:简介:衰老和高血压会增加勃起功能障碍(ED)和心血管疾病的风险。动脉供血不足可能是高血压相关性ED的主要因素。考虑到内部阴部动脉在控制阴茎血管阻力方面占主导地位,该血管的病理变化对于诱导老年高血压患者的ED至关重要。目的:我们评估了与年龄有关的高血压及其治疗对年轻和老龄自发性高血压大鼠(SHRs)的勃起功能和阴部动脉结构的影响。方法:使用阿扑吗啡(80 mg / kg)在15周和77周龄的SHR和Wistar Kyoto(WKY)大鼠中监测勃起反应。处死时,对血管系统进行灌注固定,并使用光镜和电子显微镜对形态进行评估,以评估主动脉,肾,肠系膜和阴部内动脉。另一组为期15周的SHR接受依那普利和氢氯噻嗪(30 mg / kg /天,2周)治疗,停药2周,然后用形态计量学评估相同的血管。使用无线电遥测法测定动脉压。主要指标:勃起功能,血管形态(管腔直径,壁厚,横截面积,细胞外基质[ECM])和动脉压。结果:年轻的SHR和WKY的勃起反应相似(1.7 +/- 0.80对1.4 +/- 0.85),但在老年SHR中显着下降(0.3 +/- 0.49)。 SHR中的血管老化与明显的阴部重塑有关,其特征在于明显的新内膜增生和内部弹性层的破坏。这种重塑涉及中间层的增厚(35 +/- 6.0微米vs. 81 +/- 3.5微米,P <0.01),管腔直径减小(282 +/- 6.3微米vs. 250 +/- 12.4微米,P < 0.05)和增加的ECM(10 +/- 2.0 microm(2)与26 +/- 10.6 microm(2),P <0.001)。在古老的阴部,内膜和新内膜边界处有明显更多的圆形合成平滑肌细胞。降压治疗降低了年轻SHR阴部动脉壁(管腔)的比率(-17%)。结论:ED伴有SHR的血管衰老涉及阴部内动脉独特的致病性重塑。在年轻的SHR中,短暂的降压治疗能够使这种异常形态退退。

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