Bone Loss in Rats with Aldosteronism

Runyan, Aliye L.; Chhokar, Vikram S.; Sun, Yao; Weber, Karl T.; Runyan, John W.; Bhattacharya, Syamal K.

doi:10.1097/00000441-200507000-00001

Cited by 30 publications

(18 citation statements)

References 54 publications

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“…Bottom: AldoST-induced gp91 phox activity was attenuated (arrow), but not prevented, by prior PTx. reverses these losses and preserves bone health (78). The negative impact of non-K ϩ -sparing diuretics on morbidity and mortality in patients with CHF has been called into question (19).…”

Section: Discussionmentioning

confidence: 99%

Calcium paradox of aldosteronism and the role of the parathyroid glands

Vidal¹,

Sun²,

Bhattacharya³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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The hypercalciuria and hypermagnesuria that accompany aldosteronism contribute to a fall in plasma ionized extracellular Ca2+ and Mg2+ concentrations ([Ca2+]o and [Mg2+]o). Despite these losses and the decline in extracellular levels of these cations, total intracellular and cytosolic free Ca2+ concentration ([Ca2+]i) is increased and oxidative stress is induced. This involves diverse tissues, including peripheral blood mononuclear cells (PBMC) and plasma. The accompanying elevation in plasma parathyroid hormone (PTH) and reduction in bone mineral density caused by aldosterone (Aldo)-1% NaCl treatment (AldoST) led us to hypothesize that Ca2+ loading and altered redox state are due to secondary hyperparathyroidism (SHPT). Therefore, we studied the effects of total parathyroidectomy (PTx). In rats receiving AldoST, without or with a Ca2+-supplemented diet and/or PTx, we monitored urinary Ca2+ and Mg2+ excretion; plasma [Ca2+]o, [Mg2+]o, and PTH; PBMC [Ca2+]i and H2O2 production; plasma alpha1-antiproteinase activity; total Ca2+ and Mg2+ in bone, myocardium, and rectus femoris; and gp91(phox) labeling in the heart. We found that 1) the hypercalciuria and hypermagnesuria and decline (P < 0.05) in plasma [Ca2+]o and [Mg2+]o that occur with AldoST were not altered by the Ca2+-supplemented diet alone or with PTx; 2) the rise (P < 0.05) in plasma PTH with AldoST, with or without the Ca2+-supplemented diet, was prevented by PTx; 3) increased (P < 0.05) PBMC [Ca2+]i and H2O2 production, increased total Ca2+ in heart and skeletal muscle, and fall in bone Ca2+ and Mg2+ and plasma alpha1-antiproteinase activity with AldoST were abrogated (P < 0.05) by PTx; and 4) gp91(phox) activation in right and left ventricles at 4 wk of AldoST was attenuated by PTx. AldoST is accompanied by SHPT, with parathyroid gland-derived calcitropic hormones being responsible for Ca2+ overload in diverse tissues and induction of oxidative stress. SHPT plays a permissive role in the proinflammatory vascular phenotype.

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Section: Discussionmentioning

confidence: 99%

Calcium paradox of aldosteronism and the role of the parathyroid glands

Vidal¹,

Sun²,

Bhattacharya³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…Animal studies(58, 59) and several human observational studies in primary aldosteronism have supported the concern that primary aldosteronism may result in declines in bone mineral density and an increased risk for fracture. Salcuni et al .…”

Section: Introductionmentioning

confidence: 96%

The renin–angiotensin–aldosterone system and calcium-regulatory hormones

2015

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There is increasing evidence of a clinically relevant interplay between the renin-angiotensin-aldosterone system and calcium regulatory systems. Classically, the former is considered a key regulator of sodium and volume homeostasis while the latter is most often associated with skeletal health. However, emerging evidence suggests an overlap in regulatory control. Hyperaldosteronism and hyperparathyroidism represent pathophysiologic conditions that may contribute to or perpetuate each other; aldosterone regulates parathyroid hormone and associates with adverse skeletal complications, and parathyroid hormone regulates aldosterone and associates with adverse cardiovascular complications. As dysregulation in both systems is linked to poor cardiovascular and skeletal health, it is increasingly important to fully characterize how they interact in order to more precisely understand their impact on human health and potential therapies to modulate these interactions. This review describes the known clinical interactions between these two systems including observational and interventional studies. Specifically, we review studies describing the inhibition of renin activity by calcium and vitamin D, and a potentially bidirectional and stimulatory relationship between aldosterone and parathyroid hormone. Deciphering these relationships might clarify variability in outcomes research, inform the design of future intervention studies, and provide insight into the results of prior and on-going intervention studies. However, before these opportunities can be addressed, more effort must be placed on shifting observational data to the proof of concept phase. This will require reallocation of resources to conduct interventional studies and secure the necessary talent.

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“…(6) Furthermore, in an animal model with aldosteronism, due to aldosterone/salt treatment, loss of minerals and progressive reduction of cortical bone strength was observed, (7) subsequently rescued by spironolactone treatment. (8)(9)(10)(11) The aim of our study was to evaluate bone involvement in patients with primary aldosteronism (PA) consecutively recruited among the patients with adrenal incidentaloma (AI) referred to two tertiary care centers in Italy.…”

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confidence: 99%

Bone involvement in aldosteronism

Salcuni

Palmieri

Carnevale

et al. 2012

Journal of Bone and Mineral Research

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In rats with aldosteronism, a reduction of bone mineral density (BMD) and cortical bone strength has been reported. Our study was aimed to evaluate bone involvement in patients with primary aldosteronism (PA). A total of 188 consecutive subjects with adrenal incidentaloma, observed between November 2009 and October 2011, were screened for PA with aldosterone-to-renin ratio. After confirmatory tests, in those who screened positive, 11 patients were diagnosed as PA and 15 patients were not (nPA). A serum/urinary biochemical profile, parathyroid hormone (PTH), BMD measured at lumbar spine (LS) and total and femoral neck (TN and FN) by dual X-ray absorptiometry, and conventional spinal radiographs (T 4 -L 4 ) were obtained in all subjects. PA patients had a significantly higher 24-hour urinary calcium (6.28 AE 1.85 versus 4.28 AE 1.18 mmol/d; p < 0.01), and PTH (9. 8 [5.8-14.6 p ¼ 0.012; and OR, 30.4; 95%CI,, p ¼ 0.045, respectively) regardless of age, body mass index (BMI), and LS-BMD. In 9 of 11 PA patients, 6 months after beginning of treatment (surgery or spironolactone) there was a significant reduction of urinary calcium excretion (p < 0.01) and PTH (p < 0.01), whereas in 5 of 11 PA patients, 1 year after beginning of treatment, BMD was significantly increased at LS, p < 0.01). In conclusion, PA is associated with osteoporosis, vertebral fractures, and increased urinary calcium excretion. ß

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Bone Loss in Rats with Aldosteronism

Cited by 30 publications

References 54 publications

Calcium paradox of aldosteronism and the role of the parathyroid glands

Calcium paradox of aldosteronism and the role of the parathyroid glands

The renin–angiotensin–aldosterone system and calcium-regulatory hormones

Bone involvement in aldosteronism

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