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[高血压与骨质疏松症]

[Hypertension and osteoporosis].

作者信息

Nakagami Hironori, Morishita Ryuichi

机构信息

Division of Vascular Medicine and Epigenetics, Osaka University United Graduate School of Child Development, Japan.

出版信息

Clin Calcium. 2013 Apr;23(4):497-503.

Abstract

The number of patients with high blood pressure and osteoporosis are increased year by year in our society. In hypertension patients, excess urinary calcium secretion induces secondary parathyroidism to increase serum calcium level by calcium release from bone, which may accelerate osteoporosis. In this aspect, there are several reports that anti-hypertensive drugs, especially thiazides, increase bone mineral density and decrease the incidence of bone fracture. In addition, we demonstrated that renin-angiotensin system can be involved in the process of osteoporosis. Angiotensin II significantly induced the expression of RANKL (receptor activator of NF-κB ligand) in osteoblasts, leading to the activation of osteoclasts, while these effects were completely blocked by an Ang II type 1 receptor blockade. Recently, it has been reported that angiotensin receptor blockade clinically decreased the incidence of bone fracture. Renin-angiotensin system might be common molecule to regulate both hypertension and osteoporosis.

摘要

在我们的社会中,高血压和骨质疏松症患者的数量逐年增加。在高血压患者中,尿钙分泌过多会诱发继发性甲状旁腺功能亢进,通过骨钙释放来提高血清钙水平,这可能会加速骨质疏松。在这方面,有几份报告指出,抗高血压药物,尤其是噻嗪类药物,可增加骨矿物质密度并降低骨折发生率。此外,我们证明肾素 - 血管紧张素系统可能参与骨质疏松症的发病过程。血管紧张素II可显著诱导成骨细胞中RANKL(核因子κB受体激活剂配体)的表达,从而导致破骨细胞活化,而这些作用可被1型血管紧张素II受体阻滞剂完全阻断。最近有报道称,血管紧张素受体阻滞剂在临床上可降低骨折发生率。肾素 - 血管紧张素系统可能是调节高血压和骨质疏松症的共同分子。

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