Bone loss in rats with aldosteronism

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

Research output: Contribution to journalArticle

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Abstract

Objective: We hypothesized that aldosteronism is accompanied by hypercalciuria and hypermagnesuria that lead to bone loss, which could be rescued By hydrochlorothiazide and spironolactone. Methods: We monitored 24-hour urinary Ca2+ and Mg2+ excretion; plasma ionized [Ca 2+]o and [Mg2+]o and plasma K +; and bone mineral density of the femur. The following groups (n = 5 in each group) were studied: age- and gender-matched, untreated controls; controls + 4 weeks hydrochlorothiazide; 4 weeks aldosterone/salt treatment (ALDOST, 0.75 μg/h and dietary 1% NaCl/0.4% KCl); 4 weeks ALDOST + hydrochlorothiazide (50 mg/kg in prepared food); and 4 weeks ALDOST + hydrochlorothiazide + spironolactone (200 mg/kg day in divided doses by twice-daily gavage). Results: ALDOST increased (P <0.05) urinary Ca 2+ and Mg2+ excretion four- and twofold, respectively; hydrochlorothiazide co-treatment attenuated (P <0.05) Ca2+ excretion in controls and during ALDOST without affecting augmented Mg 2+ excretion whereas hydrochlorothiazide + spironolactone normalized Ca2+ and reduced Mg2+ excretion (P <0.05). Compared with controls, plasma [Ca2+]o at 4 weeks of ALDOST was reduced (0.89 ± 0.02 versus 0.83 ± 0.03 mmol/L; P <0.05) but remained no different from levels in controls with hydrochlorothiazide and hydrochlorothiazide + spironolactone (0.88 ± 0.04 and 0.97 ± 0.03 mmol/L, respectively). Plasma [Mg2+]o fell (P <0.05) with ALDOST + hydrochlorothiazide (0.23 ± 0.01 versus 0.34 ± 0.01 mmol/L) and was prevented with spironolactone co-treatment (0.33 ± 0.01 mmol/dL). Hypokalemia (2.9 ± 0.2 mmol/L) occurred in rats with ALDOST + hydrochlorothiazide but not with spironolactone co-treatment. At 4 weeks of ALDOST, plasma parathyroid hormone was increased (30 ± 4 versus 11 ± 3 pg/mL; P <0.05) and bone mineral density was reduced (0.153 ± 0.006 versus 0.170 ± 0.002 g/cm2; P <0.05). Co-treatments with either hydrochlorothiazide or hydrochlorothiazide + spironolactone each prevented bone loss. Conclusions: Hypercalciuria and hypermagnesuria accompany aldosteronism and account for a decline in their plasma ionized concentrations and secondary hyperparathyroidism with bone resorption. Attenuation of bone loss in aldosteronism can be achieved with hydrochlorothiazide; however, mono- and divalent cation homeostasis, together with bone integrity, are each preserved with the combination hydrochlorothiazide + spironolactone.

Original languageEnglish (US)
Pages (from-to)1-7
Number of pages7
JournalAmerican Journal of the Medical Sciences
Volume330
Issue number1
DOIs
StatePublished - Jan 1 2005

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Hyperaldosteronism
Hydrochlorothiazide
Bone and Bones
Hypercalciuria
Spironolactone
Bone Density
Monovalent Cations
Secondary Hyperparathyroidism
Hypokalemia
Divalent Cations
Bone Resorption
Aldosterone
Parathyroid Hormone
Femur
spironolactone drug combination buthiazide
Homeostasis
Salts
Food

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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Bone loss in rats with aldosteronism. / Runyan, Aliye L.; Chhokar, Vikram S.; Sun, Yao; Bhattacharya, Syamal; Runyan, John W.; Weber, Karl.

In: American Journal of the Medical Sciences, Vol. 330, No. 1, 01.01.2005, p. 1-7.

Research output: Contribution to journalArticle

Runyan, Aliye L. ; Chhokar, Vikram S. ; Sun, Yao ; Bhattacharya, Syamal ; Runyan, John W. ; Weber, Karl. / Bone loss in rats with aldosteronism. In: American Journal of the Medical Sciences. 2005 ; Vol. 330, No. 1. pp. 1-7.
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title = "Bone loss in rats with aldosteronism",
abstract = "Objective: We hypothesized that aldosteronism is accompanied by hypercalciuria and hypermagnesuria that lead to bone loss, which could be rescued By hydrochlorothiazide and spironolactone. Methods: We monitored 24-hour urinary Ca2+ and Mg2+ excretion; plasma ionized [Ca 2+]o and [Mg2+]o and plasma K +; and bone mineral density of the femur. The following groups (n = 5 in each group) were studied: age- and gender-matched, untreated controls; controls + 4 weeks hydrochlorothiazide; 4 weeks aldosterone/salt treatment (ALDOST, 0.75 μg/h and dietary 1{\%} NaCl/0.4{\%} KCl); 4 weeks ALDOST + hydrochlorothiazide (50 mg/kg in prepared food); and 4 weeks ALDOST + hydrochlorothiazide + spironolactone (200 mg/kg day in divided doses by twice-daily gavage). Results: ALDOST increased (P <0.05) urinary Ca 2+ and Mg2+ excretion four- and twofold, respectively; hydrochlorothiazide co-treatment attenuated (P <0.05) Ca2+ excretion in controls and during ALDOST without affecting augmented Mg 2+ excretion whereas hydrochlorothiazide + spironolactone normalized Ca2+ and reduced Mg2+ excretion (P <0.05). Compared with controls, plasma [Ca2+]o at 4 weeks of ALDOST was reduced (0.89 ± 0.02 versus 0.83 ± 0.03 mmol/L; P <0.05) but remained no different from levels in controls with hydrochlorothiazide and hydrochlorothiazide + spironolactone (0.88 ± 0.04 and 0.97 ± 0.03 mmol/L, respectively). Plasma [Mg2+]o fell (P <0.05) with ALDOST + hydrochlorothiazide (0.23 ± 0.01 versus 0.34 ± 0.01 mmol/L) and was prevented with spironolactone co-treatment (0.33 ± 0.01 mmol/dL). Hypokalemia (2.9 ± 0.2 mmol/L) occurred in rats with ALDOST + hydrochlorothiazide but not with spironolactone co-treatment. At 4 weeks of ALDOST, plasma parathyroid hormone was increased (30 ± 4 versus 11 ± 3 pg/mL; P <0.05) and bone mineral density was reduced (0.153 ± 0.006 versus 0.170 ± 0.002 g/cm2; P <0.05). Co-treatments with either hydrochlorothiazide or hydrochlorothiazide + spironolactone each prevented bone loss. Conclusions: Hypercalciuria and hypermagnesuria accompany aldosteronism and account for a decline in their plasma ionized concentrations and secondary hyperparathyroidism with bone resorption. Attenuation of bone loss in aldosteronism can be achieved with hydrochlorothiazide; however, mono- and divalent cation homeostasis, together with bone integrity, are each preserved with the combination hydrochlorothiazide + spironolactone.",
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TY - JOUR

T1 - Bone loss in rats with aldosteronism

AU - Runyan, Aliye L.

AU - Chhokar, Vikram S.

AU - Sun, Yao

AU - Bhattacharya, Syamal

AU - Runyan, John W.

AU - Weber, Karl

PY - 2005/1/1

Y1 - 2005/1/1

N2 - Objective: We hypothesized that aldosteronism is accompanied by hypercalciuria and hypermagnesuria that lead to bone loss, which could be rescued By hydrochlorothiazide and spironolactone. Methods: We monitored 24-hour urinary Ca2+ and Mg2+ excretion; plasma ionized [Ca 2+]o and [Mg2+]o and plasma K +; and bone mineral density of the femur. The following groups (n = 5 in each group) were studied: age- and gender-matched, untreated controls; controls + 4 weeks hydrochlorothiazide; 4 weeks aldosterone/salt treatment (ALDOST, 0.75 μg/h and dietary 1% NaCl/0.4% KCl); 4 weeks ALDOST + hydrochlorothiazide (50 mg/kg in prepared food); and 4 weeks ALDOST + hydrochlorothiazide + spironolactone (200 mg/kg day in divided doses by twice-daily gavage). Results: ALDOST increased (P <0.05) urinary Ca 2+ and Mg2+ excretion four- and twofold, respectively; hydrochlorothiazide co-treatment attenuated (P <0.05) Ca2+ excretion in controls and during ALDOST without affecting augmented Mg 2+ excretion whereas hydrochlorothiazide + spironolactone normalized Ca2+ and reduced Mg2+ excretion (P <0.05). Compared with controls, plasma [Ca2+]o at 4 weeks of ALDOST was reduced (0.89 ± 0.02 versus 0.83 ± 0.03 mmol/L; P <0.05) but remained no different from levels in controls with hydrochlorothiazide and hydrochlorothiazide + spironolactone (0.88 ± 0.04 and 0.97 ± 0.03 mmol/L, respectively). Plasma [Mg2+]o fell (P <0.05) with ALDOST + hydrochlorothiazide (0.23 ± 0.01 versus 0.34 ± 0.01 mmol/L) and was prevented with spironolactone co-treatment (0.33 ± 0.01 mmol/dL). Hypokalemia (2.9 ± 0.2 mmol/L) occurred in rats with ALDOST + hydrochlorothiazide but not with spironolactone co-treatment. At 4 weeks of ALDOST, plasma parathyroid hormone was increased (30 ± 4 versus 11 ± 3 pg/mL; P <0.05) and bone mineral density was reduced (0.153 ± 0.006 versus 0.170 ± 0.002 g/cm2; P <0.05). Co-treatments with either hydrochlorothiazide or hydrochlorothiazide + spironolactone each prevented bone loss. Conclusions: Hypercalciuria and hypermagnesuria accompany aldosteronism and account for a decline in their plasma ionized concentrations and secondary hyperparathyroidism with bone resorption. Attenuation of bone loss in aldosteronism can be achieved with hydrochlorothiazide; however, mono- and divalent cation homeostasis, together with bone integrity, are each preserved with the combination hydrochlorothiazide + spironolactone.

AB - Objective: We hypothesized that aldosteronism is accompanied by hypercalciuria and hypermagnesuria that lead to bone loss, which could be rescued By hydrochlorothiazide and spironolactone. Methods: We monitored 24-hour urinary Ca2+ and Mg2+ excretion; plasma ionized [Ca 2+]o and [Mg2+]o and plasma K +; and bone mineral density of the femur. The following groups (n = 5 in each group) were studied: age- and gender-matched, untreated controls; controls + 4 weeks hydrochlorothiazide; 4 weeks aldosterone/salt treatment (ALDOST, 0.75 μg/h and dietary 1% NaCl/0.4% KCl); 4 weeks ALDOST + hydrochlorothiazide (50 mg/kg in prepared food); and 4 weeks ALDOST + hydrochlorothiazide + spironolactone (200 mg/kg day in divided doses by twice-daily gavage). Results: ALDOST increased (P <0.05) urinary Ca 2+ and Mg2+ excretion four- and twofold, respectively; hydrochlorothiazide co-treatment attenuated (P <0.05) Ca2+ excretion in controls and during ALDOST without affecting augmented Mg 2+ excretion whereas hydrochlorothiazide + spironolactone normalized Ca2+ and reduced Mg2+ excretion (P <0.05). Compared with controls, plasma [Ca2+]o at 4 weeks of ALDOST was reduced (0.89 ± 0.02 versus 0.83 ± 0.03 mmol/L; P <0.05) but remained no different from levels in controls with hydrochlorothiazide and hydrochlorothiazide + spironolactone (0.88 ± 0.04 and 0.97 ± 0.03 mmol/L, respectively). Plasma [Mg2+]o fell (P <0.05) with ALDOST + hydrochlorothiazide (0.23 ± 0.01 versus 0.34 ± 0.01 mmol/L) and was prevented with spironolactone co-treatment (0.33 ± 0.01 mmol/dL). Hypokalemia (2.9 ± 0.2 mmol/L) occurred in rats with ALDOST + hydrochlorothiazide but not with spironolactone co-treatment. At 4 weeks of ALDOST, plasma parathyroid hormone was increased (30 ± 4 versus 11 ± 3 pg/mL; P <0.05) and bone mineral density was reduced (0.153 ± 0.006 versus 0.170 ± 0.002 g/cm2; P <0.05). Co-treatments with either hydrochlorothiazide or hydrochlorothiazide + spironolactone each prevented bone loss. Conclusions: Hypercalciuria and hypermagnesuria accompany aldosteronism and account for a decline in their plasma ionized concentrations and secondary hyperparathyroidism with bone resorption. Attenuation of bone loss in aldosteronism can be achieved with hydrochlorothiazide; however, mono- and divalent cation homeostasis, together with bone integrity, are each preserved with the combination hydrochlorothiazide + spironolactone.

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