Increased calcium and magnesium excretion induced by lithium carbonate

Andreoli, V. M.; Villani, F; Brambilla, G.

doi:10.1007/bf00422619

Cited by 25 publications

(14 citation statements)

References 23 publications

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“…Our data support the hypothesis that the previously reported systemic effects of lithium on mineral metabolism in man and experimental animal models (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) may be a function of the varying skeletal response to the lithium ion. …”

Section: Discussionsupporting

confidence: 90%

“…The response of serum magnesium of animals treated with lithium has also been controversial with both normal Received for publication 8 September 1977 and in revised form 16 March 1978. (7,8) and elevated (9) values recorded. Moreover, both enhanced (13) and inhibited (14) phosphaturic responses to parathyroid hormone have been attributed to this ion.…”

Section: Introductionmentioning

confidence: 86%

“…Lithium treatment in man has been reported to induce hypercalcemia with elevated levels of parathyroid hormone and magnesium (2), hypocalciuria without alterations in response to parathyroid hormone (3)(4)(5), and renal tubular acidosis (6). In the rat, lithium has been noted to have no effect on serum calcium (7,8) or to result in hypercalcemia (9) and hypercalciuria (9)(10)(11)(12). The response of serum magnesium of animals treated with lithium has also been controversial with both normal Received for publication 8 September 1977 and in revised form 16 March 1978.…”

Section: Introductionmentioning

confidence: 99%

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Lithium inhibition of bone mineralization and osteoid formation.

Baran¹,

Schwartz²,

Bergfeld³

et al. 1978

J. Clin. Invest.

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A B S T R A C T Lithium chloride administration to growing rats, which resulted in circulating lithium levels of 1.4 meq/liter, was attended by significant suppression of bone mineralization and organic matrix synthesis as assessed by tetracycline labeling and histological quantitation of osteoid, respectively. These effects of lithium were not associated with changes in animal behavior, nor were there any significant differences in blood levels of calcium, phosphorus, alkaline phosphatase, creatinine, pH, or parathyroid hormone. The data suggest that lithium inhibition of bone mineralization is secondary to suppression of osteoid formation.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

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Lithium inhibition of bone mineralization and osteoid formation.

Baran¹,

Schwartz²,

Bergfeld³

et al. 1978

J. Clin. Invest.

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“…A number of reports have shown that lithium treatment is accompanied by increased plasma magnesium concentrations (Nielsen, 1964;Bunney, Goodwin, Davies & Fawcett, 1968;Aronoff et al 1971;Andreoli et al 1972;Birch & Jenner, 1973;Mellerup et al 1973). Birch & Jenner (1973) reported that in rats lithium apparently leads to a reduction in brain magnesium at the same time that plasma magnesium levels are increased.…”

Section: Discussionmentioning

confidence: 99%

The effect of lithium on electrolyte transport by the in situ choroid plexus of the cat.

Reed¹,

Yen²

1980

The Journal of Physiology

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SUMMARY1. The effects of lithium on electrolyte transport were studied by using the cat choroid plexus isolated in a chamber in situ.2. Lithium infused intravenously to produce plasma lithium concentrations up to 5 m-equiv/l. caused an increase in plasma magnesium with no effect on the concentration of magnesium in the chamber fluid.3. When 22NaCl was infused intravenously the chamber fluid/plasma ratio of 22Na was nearly 1 in the first 30 min sample and at the steady state it was significantly greater than 1.4. When lithium chloride (1-5 m-equiv/l.) or potassium chloride (6.6 m-equiv/l.) was added to the chamber at the start of a collection period with plasma 22Na in the steady state, the 22Na content of the chamber fluid promptly increased 118 and 68 %, respectively, above the control value with no increase in secretary rate.5. The addition of ouabain to the chamber fluid, in addition to the lithium chloride or potassium chloride, tended to stimulate or have no significant effect on 22Na uptake at a concentration of 10-5 M and to reduce it as well as the secretary rate at 10-3 M.6. The data are compatible with there being two functionally separate sodium transport systems in the choroid plexus. One transports sodium accompanied by an anion and water to provide the fluid secreted into the chamber (c.s.f.) and the other operates primarily to regulate the potassium concentration of the c.s.f. by pumping potassium out in exchange for sodium.7. Lithium can be transported by both systems to a limited extent and the presence of lithium in the c.s.f. stimulates the sodium-potassium regulating pump.

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“…Previous studies have indicated that lithium has an effect on calcium metab olism (1,2). The possibility therefore exists that such an influence may have certain bearing on the effect of lithium in manic-depressive psychosis, because calcium is important both for the impulse propagation along the nerve cell (3) and for the synaptic transmission (4).…”

Section: Introductionmentioning

confidence: 99%