SCOR IN HYPERTENSION

波士顿大学高血压专业研究中心将 提供广泛和多学科的方法来研究 细胞和分子机制参与发病机制和 高血压的并发症。 该计划的一个主要目标将是确定钠的作用， 体液因素及其相互关系在青光眼发病机制中的作用 高血压。这些研究将包括：a)调查 培养的延髓上皮细胞钠转运的调节 正常血压和高血压患者的细胞和动脉平滑肌细胞 大鼠；b)19-去氧皮质酮对血液升高的贡献 人体内的压力和高血压的实验形式；c) 钠泵与Na、K-异构体的表达与调控 高血压动物模型心脏、动脉等组织中的ATPase； D)有很强家族病史的高血压患者的遗传学研究 以确定该病是否存在限制性片段长度 新近发现的Na，K-ATPaseα-1亚型的多态性 我们在达尔盐敏症和自发性高血压患者中 菌株；e)血管紧张素II受体的克隆和特性， 它们的组织调节，以及它们在高血压中的潜在作用；f) 缓激肽的作用及其与其他血管活性系统的相互作用 利用一种新的、相对的 本实验室研制的缓激肽特异性抑制剂；g) 在完整的动脉和培养的血管细胞中激肽释放酶-激动素系统，以及 该系统各组成部分的表达、它们的调节和反应 和h)V1和V2类加压素的重要性 人和实验性高血压和心力衰竭的受体 这些受体的特异性抑制剂已经在我们的 实验室。 研究的另一个主要重点也将是通过 高血压和高胆固醇血症会导致动脉损伤和 动脉硬化。选定的生长因子和 将检查结缔组织成分以确定自分泌 旁分泌相互作用参与血管疾病的发展。 低氧致动脉环功能异常的原因探讨 高血压和高胆固醇血症将被评估和他们的 与G蛋白和生长因子变化的关系将是 下定决心。此外，心肌肥厚对心脏的影响 离体心的结构和功能及其对心脏的反应 将对潜在的有害刺激进行研究。 高血压症状自评量表应为病因提供重要的新知识 和高血压的后果，应该导致对其进行新的治疗 预防和治疗。

The Hypertension Specialized Center of Research at Boston University will provide a broad-based and multidisciplinary approach to the study of cellular and molecular mechanisms involved in the pathogenesis and complications of hypertension. A major goal of the program will be to determine the role of sodium, humoral factors, and their interrelationships in the etiology of hypertension. These studies will include investigation of: a) the regulation of sodium transport in cultured rental medullary epithelial cells and arterial smooth muscle cells from normotensive and hypertensive rats; b) the contribution of 19-nor-deoxycorticosterone to elevated blood pressure in human and experimental forms of hypertension; c) the role of the sodium pump and the expression and regulation of the isoforms of Na, K- ATPase in heart, artery, and other tissues of hypertensive animal models; d) genetic studies in hypertensive patients with a strong family history of the disease to determine the presence of a restriction fragment length polymorphism of the alpha-1 isoform of Na, K-ATPase demonstrated recently by us in both the Dahl salt-sensitive and spontaneously hypertensive strains; e) the cloning and characterization of angiotensin II receptors, their tissue regulation, and their potential role in hypertension; f) the role of bradykinin and its interaction with other vaso-active systems in cardiovascular hemodynamics and hypertension utilizing a new, relatively specific inhibitor of bradykinin prepared in our laboratory; g) the kallikrein-kinin system in intact arteries and cultured vascular cells, and the expression of components of this system, their regulation, and response to hypertension; and h) the importance of V1 and V2 classes of vasopressin receptors in human and experimental hypertension and heart failure using specific inhibitors of these receptors which have been prepared in our laboratory. Another major emphasis of the studies also will be on the mechanisms by which hypertension and hypercholesterolemia induce arterial injury and atherosclerosis. The expression of selected growth factors and of connective tissue components will be examined to determine the autocrine and paracrine interactions involved in the development of vascular disease. The cause of functional abnormalities in arterial rings induced by hypertension and hypercholesterolemia will be assessed and their relationship to changes in G-proteins and growth factors will be determined. Furthermore, the effects of cardiac hypertrophy on cardiac structure and function and on the response of isolated hearts to potentially injurious stimuli will be studied. The Hypertension SCOR should provide important new knowledge on the causes and consequences of hypertension and should lead to new approaches on its prevention and treatment.