SCOR IN HYPERTENSION

这项多学科的SCOR提案继续侧重于 高血压中的心脏，强调细胞、生化和功能 心脏参与高血压发病机制的研究进展 心血管疾病。提出的几项建议的广泛目标 研究是确定生物化学或神经体液机制 高血压性心脏肥厚的发生发展及其机制 充血性心力衰竭的最终命运以及心脏和心脏的作用 血管在高血压疾病的发展过程中起着重要作用。这位大姐 目标在五个提案中执行，其中四个提案专门关注 关于心脏：(1)激活心脏的机制研究 心肌肾素-血管紧张素系统及其生理学相关性 心血管功能；(2)高血压患者钙调节的研究 肥大；(3)伸展或其他刺激的翻译机制 从心脏分泌颗粒释放心钠素；以及(4)作用 盐敏感症患者心脏和外周压力感受器的变化 并进一步探索心脏可能在其中发挥作用的范式 在调节血压水平方面发挥积极作用。最后， 血压控制与高血压发展之间的脱节 心肌肥厚也见于周围性心肌肥厚。 血管肥大可能是肾脏恶化的原因 肾动脉狭窄患者的功能。这一假设是 外科与内科前瞻性随机研究的基础 建议治疗的解剖性肾动脉狭窄 继续和完成这一《公约》续期。 从这些众多的研究，从最基础的到非常实用的临床 水平，我们应该大大推进我们的目标，理解 血管紧张素转换酶对动脉高血压危害的发病机制 对治疗的切实影响。

This multidisciplinary SCOR proposal continues to focus on the role of the heart in hypertension with emphasis on cellular, biochemical and functional mechanisms whereby the heart participates in pathogenesis of hypertensive cardiovascular disease. The broad objectives of the several proposed studies is to determine the biochemical or neurohumoral mechanisms that underlie the development of hypertensive hypertrophy of the heart and its ultimate fate in congestive heart failure as well as the role the heart and vessels play in the progression of hypertensive disease. This broad objective is carried out in five proposals, four of which focus exclusively on the heart: (1) studies of the mechanisms involved in activation of the myocardial renin angiotensin system and their physiologic relevance to cardiovascular function; (2) studies of calcium regulation in hypertensive hypertrophy; (3) mechanisms whereby stretch or other stimuli are translated into release of ANF from secretory granules in the heart; and (4) the role of the cardiac and peripheral baroreceptors in patients with salt sensitive hypertension and explores further the paradigm in which the heart may play a active role in the modulation of blood pressure levels. Finally, the dissociation between blood pressure control and the development of myocardial hypertrophy is also found in the persistence of peripheral vascular hypertrophy and may be responsible for the deterioration of renal function in patients with renal artery stenosis. This hypothesis was the basis for the prospective randomized study of surgical versus medical treatment of anatomic renal artery stenosis that is being proposed for continuation and completion in this SCOR renewal. From these many studies, at the most basic to the very applied clinical levels, we should substantially further our goals of understanding the pathogenesis of the deleterious effects of arterial hypertension with tangible implications for therapy.