ETIOLOGY AND PATHOPHYSIOLOGY OF AUTONOMIC FAILURE

自主神经衰竭的病因学和病理生理学

• 批准号: 7375559
• 负责人: Italo Biaggioni
• 金额: $ 28.57万
• 依托单位: VANDERBILT UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-12-01 至 2006-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7375559
• 关键词: ETIOLOGY; PATHOPHYSIOLOGY; AUTONOMIC; FAILURE; ETIOLOGY; PATHOPHYSIOLOGY; AUTONOMIC; FAILURE

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. Instantaneous changes in blood pressure, such as those produced by assuming the upright posture, are regulated to a large extent by the autonomic nervous system. Patients suffering from autonomic failure lose these buffering capacity and are unable to compensate for venous pooling associated with standing. The more severe patients faint every time they attempt standing, because of profound orthostatic hypotension. Of interest, our studies indicate that approximately 50% of these patients have supine hypertension, which is entirely accounted for by an increased in systemic vascular resistance even in patients with very low plasma norepinephrine and virtually undetectable plasma renin activity. Our main objective is to understand the factor(s) driving this increased vascular resistance. Our underlying hypothesis is that understanding the mechanisms hypertension in autonomic failure will contribute to our understanding of cardiovascular regulation in general,and human hypertension in particular.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。自主神经系统在很大程度上调节了血压的瞬时变化，例如假设直立姿势产生的瞬时变化。患有自主衰竭的患者失去了这些缓冲能力，无法补偿与站立相关的静脉池。由于高度的体位性低血压，每次尝试站立时，越严重的患者都会晕倒。有趣的是，我们的研究表明，这些患者中约有50％患有仰卧高血压，即使在血浆去甲肾上腺素非常低的患者中，全身血管耐药性的增加也完全解释了，并且几乎无法检测到的血浆肾素活性。我们的主要目标是了解驱动这种增加的血管抗性的因素。我们的基本假设是，了解自主教失败的高血压机制将有助于我们对一般心血管调节的理解，尤其是人类的高血压。