高血压是多种心血管疾病的最重要的可控危险因素。钙磷代谢调节因子甲状旁腺素（PTH）在动脉钙化中起重要作用。既往研究，包括我们课题组的横断面研究发现，PTH增高与高血压密切关联。但PTH与高血压的因果关系尚不明确，机制也不十分清楚。最新研究显示PTH和肾素-血管紧张素-醛固酮系统（RAAS）存在相互作用。我们假设PTH可能和盐摄入、肾脏局部RAAS、肾脏钠转运蛋白等水盐代谢调节因素相互作用，影响高血压发病。在本项目中，我们将利用前瞻性队列明确PTH和高血压发病的因果关系，并通过随机交叉盐负荷人体试验、动物及分子水平试验等探讨PTH与盐摄入、循环和肾脏局部RAAS激活、肾脏钠盐处理异常的关系及其在高血压发生和发展中的作用及可能的机制。课题研究结果将有助于深入了解PTH在高血压发病中的作用及机制，为高血压的防治寻找新的干预靶点。

Hypertension is the most important reversible risk factor for cardiovascular diseases. Parathyroid hormone (PTH),as one of the regulators of calcium and phosphate homeostasis, plays an important role in arterial calcification. Previous cross-sectional studies , including ours, demonstrated that serum PTH level was positively and independently associated with the presence of hypertension. However, up to now the causal relationship between PTH and hypertension has not been established, and the involved mechanisms remain unclear. Recent evidence suggested that PTH interacted with the renin-angiotensin-aldosterone system (RAAS). We hypothesized that increased PTH might result in hypertension via its interaction with salt intake, local RAAS in the kidney, and renal sodium-transfering proteins. In this comprehensive project, we will first analyze the prospective data of our population cohort to examine if there is a causal relationship between PTH and incidence of hypertension. We will then investigate the role of the interaction of PTH with salt intake, circulating and local renal RAAS activation, and kidney sodium handling deficiency in the pathogenesis of hypertension by carrying out cohort studies, random crossover sodium loading studies in human, and experimental animal and molecular studies. The present project will help to understand the role of PTH in the pathogenesis of hypertension, and may help in finding a novel intervention target for hypertension.