Decrease of calcium turnover during the onset of mineralocorticoid hypertension in the rat

Stoclet, Jean‐Claude; Miss-Pages, C; Berthelot, Alain; Gairard, A.

doi:10.1016/0024-3205(75)90330-6

Cited by 13 publications

(4 citation statements)

References 10 publications

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“…These calculations were made by using previously developed equations (Marshall, 1969 ;Stoclet et al, 1975), given below : These calculations were made by using previously developed equations (Marshall, 1969 ;Stoclet et al, 1975), given below :…”

Section: Methodsmentioning

confidence: 99%

“…The calcium pool in which the tracer was diluted, and the rate of calcium transfer from this pool to the rest of the body, were calculated 3 rnin and 30 rnin after injection of the tracer, in order to provide information on fast and slower phenomena involved in calcium metabolism. These calculations were made by using previously developed equations (Marshall, 1969 ;Stoclet et al, 1975), given below :…”

Section: Methodsmentioning

confidence: 99%

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Effects of Inaktin on Calcium Metabolism in the Rat

Heitz¹,

Stoclet²

1988

Fundamemntal Clinical Pharma

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Experiments were designed to investigate further the alterations in calcium metabolism caused by inaktin, a thiobarbiturate that impairs parathyroid hormone action in rats (1981). Treatment with an anesthetic dose of inaktin induced a drop in serum calcium without any variation in immunoreactive parathyroid hormone serum level and slowed body calcium turnover as studied with 45Ca, but was without effect on blood pH or partial pressures of oxygen and carbon dioxide. In contrast, calcium metabolism in rats was unchanged after treatment with an anesthetic dose of pentothal, another thiobarbiturate anesthetic. The effect of inaktin on body calcium turnover was dose-dependent and significant even at non-anesthetic levels. A marked slowing of the fast phenomena accounting for the initial dilution of the tracer in the animal was observed, accompanied by a corresponding decrease in rapid 45Ca uptake into bone, but not other tissues. These results show that inaktin slows calcium turnover, especially the fast renewal of calcium in bone. These effects were not correlated with anesthesia or immobilization, and we suggest that inaktin-induced changes in calcium metabolism involve an impairment of hypocalcemia-induced parathyroid hormone secretion, in addition to the impairment of parathyroid hormone effects previously reported. Furthermore, the present findings suggest that inaktin might be a useful tool for investigation of the rapid mobilization of bone calcium, which is as yet not well understood.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Effects of Inaktin on Calcium Metabolism in the Rat

Heitz¹,

Stoclet²

1988

Fundamemntal Clinical Pharma

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“…Calcium metabolism was studied as described by Stoclet et al (1975). Calcium metabolism was studied as described by Stoclet et al (1975).…”

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confidence: 99%

“…of the specific activities against the logarithm of time was calculated as described by Stoclet et al (1975) to determine the average serum specific activity over 120 min (time integral of serum specific activity divided by time) and the slope h of the curve describing the fall of serum specific activity beyond 30 min after tracer injection. s.e.m.…”

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confidence: 99%

In vivo alteration of calcium turnover induced by reserpine in rat tissues

Heitz

Stoclet

1980

Journal of Pharmacy and Pharmacology

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when compared with rats injected acutely with saline. Since the apomorphine-induced sedation is considered to be mediated by presynaptic dopamine receptors, these data are evidence for the development of presynaptic supersensitivity following chronic haloperidol. Higher doses of apomorphine elevated locomotor activity to presedative levels indicating an activation of supersensitive postsynaptic dopamine receptors. In addition 2 out of 5 rats displayed obvious stereotypic behaviour.Combined injection of haloperidol and lithium daily for 34 days reversed the pre-and postsynaptic supersensitive responses to apomorphine. Apomorphine at 0.004 and 0.008 mg kg-' did not induce significant inhibition of locomotor activity as was seen in rats treated chronically with only haloperidol (Fig. 1). This supports previous electrophysiological data suggesting that lithium blocks the development of presynaptic dopamine receptor supersensitivity.The higher doses of apomorphine did not produce increases in locomotor activity in chronic haloperidol plus lithium treated rats (Fig. 1). On the contrary apomorphine (0.01 6 mg kg-l) induced sedation that was analogous to the responses seen in the control groups.In conclusion lithium appears to block the develop. ment of supersensitivity in both pre-and postsynaptic dopamine receptors. The chronic lithium regimen has been demonstrated to result in plasma lithium concen. trations in the therapeutic range of lithium in man (Allikments et al 1979). Therefore the stabilization of pre-and postsynaptic receptors by lithium may repre. sent an important mechanism in the clinical pharmacotherapy of manic-depressive disorders and tardive dyskinesia.

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