MECHANISMS OF NOCTURNAL HYPERTENSION IN TYPE 1 DIABETES

1 型糖尿病夜间高血压的机制

• 批准号: 7604290
• 负责人: DANIEL BATLLE
• 金额: $ 2.88万
• 依托单位: NORTHWESTERN UNIVERSITY AT CHICAGO
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-12-01 至 2007-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7604290
• 关键词: MECHANISMS; NOCTURNAL; HYPERTENSION; TYPE; DIABETES

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. Diabetes is the leading cause of end-stage renal disease (ESRD) world-wide. In susceptible individuals, the development of renal microvascular complications in type 1 diabetics often follows a uniform pattern which initially is asymptomatic with normal renal, cardiovascular and autonomic function. Progression of renal disease is then characterized by the development of nocturnal hypertension and microalbuminuria(MA). These changes are subsequently followed by the development of overt hypertension and proteinuria prior to the development of ESRD. Healthy individuals typically exhibit a fall in blood pressure at night in relation to their daytime blood pressure by approximately 10-25%. An interesting feature of type 1 diabetics is the loss of this normal circadian variation in blood pressure where blood pressure does not fall at night. The etiology of this nocturnal hypertension in type 1 diabetics has been ascribed to the loss or attenuation of the circadian changes in sympatho-vagal balance usually present in healthy individuals. This circadian sympatho-vagal axis in healthy individuals appears to be controlled through the diurnal release of catecholamines and current evidence suggests that this release may potentially be modulated by circulating levels of melatonin. To date, there is limited evidence regarding catecholamine and melatonin levels in type 1 diabetics. The question therefore arises if the altered sympatho-vagal axis of type 1 diabetics is the result of altered levels of nocturnal melatonin and catecholamine release. Specific Aim #1: To determine if type 1 diabetics with nocturnal hypertension have a significantly altered level of nocturnal melatonin release when compared to a group of type 1 diabetics without nocturnal hypertension and a group of healthy controls. Specific Aim #2: To examine the sympatho-vagal balance in these same 3 groups to test the hypothesis that decreased nocturnal melatonin secretion may be associated with increased catecholamine release and altered sympatho-vagal balance in type 1 diabetics with nocturnal hypertension as compared to type 1 diabetics without nocturnal hypertension and healthy controls. Specific Aim #3: To determine if supplemental administration of melatonin significantly changes nocturnal blood pressure when given to type 1 diabetics with nocturnal hypertension.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 糖尿病是全世界终末期肾病 (ESRD) 的主要原因。 在易感个体中，1 型糖尿病患者肾微血管并发症的发展通常遵循统一的模式，最初无症状，肾脏、心血管和自主神经功能正常。 肾脏疾病的进展以夜间高血压和微量白蛋白尿（MA）的发展为特征。 这些变化随后在发展为 ESRD 之前出现明显的高血压和蛋白尿。 健康人夜间血压通常比白天血压下降约 10-25%。 1 型糖尿病患者的一个有趣特征是失去了这种正常的血压昼夜节律变化，即夜间血压不会下降。 1 型糖尿病患者夜间高血压的病因归因于健康个体中通常存在的交感迷走神经平衡昼夜节律变化的丧失或减弱。 健康个体的昼夜节律交感迷走神经轴似乎是通过儿茶酚胺的昼夜释放来控制的，目前的证据表明，这种释放可能受到褪黑激素循环水平的调节。 迄今为止，关于 1 型糖尿病患者儿茶酚胺和褪黑激素水平的证据有限。 因此，问题是，1 型糖尿病患者交感迷走轴的改变是否是夜间褪黑激素和儿茶酚胺释放水平改变的结果。 具体目标#1：确定与一组无夜间高血压的 1 型糖尿病患者和一组健康对照相比，患有夜间高血压的 1 型糖尿病患者的夜间褪黑激素释放水平是否显着改变。 具体目标#2：检查这 3 组患者的交感迷走神经平衡，以检验这样的假设：与没有夜间高血压的 1 型糖尿病患者和健康对照相比，患有夜间高血压的 1 型糖尿病患者夜间褪黑素分泌减少可能与儿茶酚胺释放增加和交感迷走神经平衡改变有关。 具体目标#3：确定患有夜间高血压的 1 型糖尿病患者补充褪黑激素是否会显着改变夜间血压。