Aldosterone enhances renal calcium reabsorption by two types of channels

Leclerc, Marie; Brunette, Michèle G.; Couchourel, Denis

doi:10.1111/j.1523-1755.2004.00725.x

Cited by 15 publications

(12 citation statements)

References 40 publications

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“…Surprisingly, CaV3.1 is also found expressed in the distal nephron of the kidney (Andreasen et al 2000), where it may be involved in Ca 2? reabsorption (Leclerc et al 2004). …”

Section: Atp-binding Cassette Transporters: the Abc Of CD 21 Efflux?mentioning

confidence: 97%

Catch me if you can! Novel aspects of cadmium transport in mammalian cells

Thévenod

2010

Biometals

157

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Cadmium (Cd(2+)) is a nonessential divalent metal ion that causes toxicity in multiple organs in humans. In order for toxicity to occur Cd(2+) must first enter cells by utilizing transport pathways for essential metals. This review focuses on studies in which Cd(2+) transport was directly demonstrated by electrophysiological, radiotracer or Cd(2+)-sensitive fluorescent dye techniques. The chemistry of Cd(2+) and metal ions in general is addressed in the context of properties relevant for transport through membrane proteins, such as hydration energy. Apart from transport by the ZIP transporters SLC39A8 and SLC39A14, which is not topic of the review, uptake of free Cd(2+) has been demonstrated for the Fe(2+)/H(+) cotransporter divalent metal transporter 1. Moreover, the multiligand endocytic receptors megalin and cubilin take up cadmium-metallothionein complexes via receptor-mediated endocytosis. The role of ATP binding cassette transporters in Cd(2+) efflux from cells is also discussed. Both the multidrug resistance-associated protein 1 and cystic fibrosis transmembrane conductance regulator are likely to transport cadmium-glutathione complexes out of cells, whereas transport of free Cd(2+) by the multidrug resistance P-glycoprotein remains controversial. Finally, arguments for and against Cd(2+) transport by Ca(2+) channels are presented. Most N- and L-type Ca(2+) channels are closed at resting membrane potential (with the exception of CaV1.3 channels) and therefore unlikely to allow significant Cd(2+) influx under physiological conditions. CaV3.1 and CaV3.2 T-type calcium channels are permeated by divalent metal ions, such as Fe(2+) and Mn(2+) because of considerable "window" currents close to resting membrane potential and could be responsible for tonic Cd(2+) entry. TRPM7 and the mitochondrial Ca(2+) uniporter are other likely candidates for Cd(2+) transporters, whereas the role of Orai proteins, the store-operated calcium channels carrying Ca(2+) release-activated Ca(2+) current, in Cd(2+) influx remains to be investigated.

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“…Surprisingly, CaV3.1 is also found expressed in the distal nephron of the kidney (Andreasen et al 2000), where it may be involved in Ca 2? reabsorption (Leclerc et al 2004). …”

Section: Atp-binding Cassette Transporters: the Abc Of CD 21 Efflux?mentioning

confidence: 97%

Catch me if you can! Novel aspects of cadmium transport in mammalian cells

Thévenod

2010

Biometals

157

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“…Although aldosterone is known to enhance Na + reabsorption by the distal nephron, its enhancement of Ca 2+ transport is a relatively new phenomenon. It appears that the effect of aldosterone on increased Ca 2+ transport in the distal luminal membranes is through L‐ and T‐type Ca 2+ channels, which require tyrosine kinase activity 168 . Another hormone that has been shown to enhance transepithelial Ca 2+ transport is arginine vasopressin 5,169 .…”

Section: Endocrine Regulation Of Ca2+ Transportmentioning

confidence: 99%

Endocrine Regulation of Calcium Transport in Epithelia

Khanal

Nemere

2008

Clin Exp Pharma Physio

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SUMMARY1. Calcium (re)absorption occurs in epithelia, including the intestine, kidney, mammary glands, placenta and gills (in the case of fish).2. Calcium is transported across epithelia by two transport mechanisms, paracellular and transcellular, and the movement is regulated by a complex array of transport processes that are mediated by hormonal, developmental and physiological factors involving the gastrointestinal tract, bone, kidney and the parathyroids.3. Clear understanding of the calcium transport pathways and their endocrine regulation is critical for minimizing various metabolic and health disorders at different physiological stages. Here, we first briefly review the calcium transport mechanisms before discussing in detail the endocrine factors that regulate calcium transport in the epithelia.

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“…Towards this, we and others have shown that high aldosterone levels are associated with high PTH levels [5][6][7][8][9]. In experimental studies it has been demonstrated that aldosterone excess increases renal and fecal loss of calcium [8][9][10]. This in turn results in secondary hyperparathyroidism which could be effectively treated by mineralocorticoid receptor (MR) blocking therapy in rats [8,9].…”

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confidence: 93%