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Relationship Between Aldosterone and Parathyroid Hormone, and the Effect of Angiotensin and Aldosterone Inhibition on Bone Health

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

Abstract

Emerging evidence suggests a stimulating effect of parathyroid hormone (PTH) on the renin–angiotensin–aldosterone system (RAAS). In primary hyperparathyroidism, chronic-elevated PTH levels seem to stimulate the RAAS which may explain the increased risk of cardiovascular disease (CVD). In addition to increased PTH levels, low vitamin D levels may also directly increase risk of CVD, as vitamin D, itself, has been shown to inhibit the RAAS. Angiotensin II, aldosterone and cortisol all negatively impact bone health. Hyperaldosteronism is associated with a reversible secondary hyperparathyroidism due to increased renal calcium excretion. Moreover, the angiotensin II receptor is expressed by human parathyroid tissue, and angiotensin may therefore directly stimulates PTH secretion. An increased bone loss is found in patients with hyperaldosteronism. The angiotensin II receptor seems main responsible for the RAAS-initiated bone loss due to a receptor activator of NF-κB ligand-mediated activation of the osteoclasts. Available data suggest a reduced fracture rate and increased bone mineral density in patients treated with angiotensin II receptor blockers, whereas treatment with angiotensin-converting enzyme inhibitors causes the opposite effects. Mineralocorticoid receptor antagonists seem to be beneficial to bone in patients with hyperaldosteronism, but it is unknown whether this also applies to other individuals. Further long-term studies are needed to clarify the effect of RAAS inhibitors on bone health. RAAS inhibitors, are widely prescribed worldwide and beneficial as well as harmful effects may have large impact on bone health in the general population.

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Abbreviations

ACEi:

Angiotensin-converting enzyme inhibitor

ACTH:

Adrenocorticotropic hormone

ALP:

Alkaline phosphatase

Ang II:

Angiotensin II

APA:

Aldosterone-producing adenoma

ARB:

Angiotensin II receptor blocker

AT1R:

Angiotensin II type 1 receptor

AT2R:

Angiotensin II type 2 receptor

BAH:

Bilateral adrenal hyperplasia

BMD:

Bone mineral density

BP:

Blood pressure

Ca:

Calcium

CVD:

Cardiovascular disease

CTx:

C-terminal telopeptide of type 1 collagen

GnRH:

Gonadotropin-releasing hormone

MR:

Mineralocorticoid receptor

MRA:

Mineralocorticoid receptor antagonist

OC:

Osteocalcin

PA:

Primary aldosteronism

PCOS:

Polycystic ovary syndrome

PTH:

Parathyroid hormone

PPHT:

Primary hyperparathyroidism

PTX:

Parathyroidectomy

SA:

Secondary aldosteronism

SHPT:

Secondary hyperparathyroidism

RAAS:

Renin–angiotensin–aldosterone system

RAASi:

RAAS inhibitors

SA:

Secondary aldosteronism

RANKL:

Receptor activator of NF-κB ligand

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Disclosures

Conflict of interest

Lise Sofie Bislev, Tanja Sikjaer, Lars Rolighed and Lars Rejnmark declare that they have no conflict of interest.

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  1. Department of Endocrinology and Internal Medicine, Tage Hansens Gade 2, Aarhus University Hospital, 8000, Aarhus C, Denmark

    Lise Sofie Bislev, Tanja Sikjær & Lars Rejnmark

  2. Department of Surgery P, Breast and Endocrine Section, Tage Hansens Gade 2, Aarhus University Hospital, 8000, Aarhus C, Denmark

    Lars Rolighed

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  1. Lise Sofie Bislev
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  2. Tanja Sikjær
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  3. Lars Rolighed
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  4. Lars Rejnmark
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Correspondence to Lise Sofie Bislev.

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Bislev, L.S., Sikjær, T., Rolighed, L. et al. Relationship Between Aldosterone and Parathyroid Hormone, and the Effect of Angiotensin and Aldosterone Inhibition on Bone Health. Clinic Rev Bone Miner Metab 13, 194–205 (2015). https://doi.org/10.1007/s12018-015-9182-0

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  • DOI: https://doi.org/10.1007/s12018-015-9182-0

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