ETIOLOGY AND PATHOPHYSIOLOGY OF AUTONOMIC FAILURE

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。 血压的瞬时变化，例如由直立姿势产生的血压，在很大程度上受到自主神经系统的调节。患有自主神经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淤积。病情较重的患者每次尝试站立时都会晕倒，因为他们患有严重的直立性低血压。有趣的是，我们的研究表明，大约50%的患者患有仰卧位高血压，这完全是 原因是全身血管阻力增加，即使在血浆去甲肾上腺素非常低且几乎检测不到血浆肾素活性的患者中也是如此。我们的主要目标是了解推动血管阻力增加的因素(S)。我们的基本假设是，理解这些机制 自主神经衰竭中的高血压有助于我们对心血管调节的一般理解，特别是对人类高血压的理解。

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.