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The Renin–Angiotensin System and Bone

  • Hypertension and bone
  • Published:
Clinical Reviews in Bone and Mineral Metabolism Aims and scope Submit manuscript

Abstract

The RAS (renin–angiotensin system) plays a key role in the regulation of blood pressure, fluid and electrolyte homeostasis and cardiovascular and renal structure and function. There is evidence that in addition to the systemic RAS the components of the RAS are expressed in the local milieu of bone, where angiotensin II increases the osteoclastogenesis while inhibit the osteoblastic activity leading to a decrease in bone mineral density. Hypertension and osteoporosis are two common diseases that frequently coexist in the elderly population, and it has been hypothesized that the activation of the local RAS might be involved in the occurrence of both diseases often seen with advancing age. Epidemiological studies have found that RAS inhibitors, including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, may exert a beneficial effect on bone mineral density, increasing the bone mass and decreasing the risk of bone fractures in patients with osteoporosis and cardiovascular diseases, and might accelerate the fracture healing process. However, both experimental and clinical studies with these RAS inhibitors led to sparse and contradictory results. Thus, in the next future a better understanding on how the components of the local RAS influence bone metabolism and remodeling will allow us to select the best therapeutic strategy for patients with osteoporosis and cardiovascular diseases.

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Acknowledgments

To Paloma Vaquero for her technical assistance.

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This review was supported by Instituto de Salud Carlos III (Red RIC, and PI11/01030) and Comunidad de Madrid (S2010/BMD-2374).

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Juan Tamargo, Ricardo Caballero, and Eva Delpón declare that they do not have any conflict of interest.

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Tamargo, J., Caballero, R. & Delpón, E. The Renin–Angiotensin System and Bone. Clinic Rev Bone Miner Metab 13, 125–148 (2015). https://doi.org/10.1007/s12018-015-9189-6

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