AUTONOMIC-SYMPATHETIC HYPERACTIVITY (AH) AND ERECTILE DYSFUNCTION

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 由于代谢综合征(MESY)在美国的患病率不断上升(23.7%)，最近受到了人们的关注，在美国，有超过4700万人受到影响。由于它与非胰岛素依赖型糖尿病(DM)、高血压(HTN)、血脂异常(DYS)、自主交感神经功能亢进(AH)和心血管疾病(CVD)有关，被认为具有巨大的社会经济代价。病理生理学研究归咎于MESY的两个关键因素：1)全身炎症(C-反应蛋白(CRP)升高)和2)自主交感神经功能亢进(AH)。MESY是勃起功能障碍(ED)的一个新的“危险因素”，因为许多异常本身就是ED的独立危险因素(即DM、HTN、DYS和CVD)。啊，作为MESY的一个组成部分，与HTN、胰岛素抵抗和DYS的发生发展有很好的关系。AH与下尿路症状(LUTS)的关系已得到证实，并推测AH可能是ED与LUTS的重要病理生理机制之一。尽管MESY的所有其他方面都是ED的关键因素，但ED和AH之间的关系完全没有被研究过。我们现在假设，在ED的发展过程中，AH是一个关键的和未被认识的病因因素，并且它在症状进展中有因果关系。为了验证这一假设，我们建议对ED患者的自主神经系统功能状态进行评估。我们建议进行一系列非侵入性评估，以反映交感神经功能，并将其与ED和阴茎动脉血流测量相关联。我们假设，患有ED的男性将在ED严重程度和AH水平增加之间存在线性关系。这项拟议的研究是一项单一地点的临床研究，其中患有勃起功能障碍的男性将接受一系列非侵入性研究，以记录自主神经张力水平、对循环应激的自主神经反应、阴茎血流、勃起功能障碍危险因素的描述和评估。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The Metabolic Syndrome (MESY) has gained recent attention due to its increasing prevalence in the US (23.7%), where it affects over 47 million people. It is thought to have great socioeconomic cost because of its association with non-insulin dependent diabetes mellitus (DM), hypertension (HTN), dyslipidemia (DYS), autonomic-sympathetic hyperactivity (AH) and cardiovascular disease (CVD). Pathophysiologic investigations blame two key components in the etiology of MESY: 1) systemic inflammation (elevated C-reactive protein (CRP)) and 2) autonomic-sympathetic hyperactivity (AH). MESY is an emerging "risk factor" for erectile dysfunction (ED) as many of the abnormalities are themselves independent risk factors for ED (i.e. DM, HTN, DYS, and CVD). AH, as a component of MESY has a well established relationship with the development of HTN, insulin resistance and DYS. A relationship between AH and Lower Urinary Tract Symptoms (LUTS) has been established, additionally it has been hypothesized that AH may be one of the crucial pathophysiologic mechanisms linking ED with LUTS. The relationship between ED and AH is completely uninvestigated even though all other aspects of the MESY are key factors for ED. We now hypothesize that AH is a crucial and unrecognized etiologic factor in the development of ED and it has a casual relationship in symptomatic progression. To test this hypothesis, we propose to make an assessment of the functional state of the autonomic nervous system in ED patients. We propose to carry out a series of non-invasive assessments that reflect sympathetic function and correlate them with ED and penile arterial flow measurements. We hypothesize that men with ED will have a linear relationship between ED severity and increasing level of AH. The proposed study is a single site clinical investigation in which men with ED will undergo a series of non-invasive studies to document the level of autonomic tone, autonomic reactivity to circulatory stress, penile blood flow, ED risk factor profiling and evaluation.