Molecular properties of calcium channels

Glossmann, Hartmut; Striessnig, Jörg

doi:10.1007/bfb0031018

Cited by 186 publications

(84 citation statements)

References 292 publications

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“…Although large amounts of Mg2" inhibit Ca2+ movement through the L-type Ca2" channel, Mg2" is not measurably permanent (44). This is supported by the observation that Ba2", which readily crosses the Ca2+ channel (17)(18)(19) does not enter through the Mg2" channel (deduced from data given here).…”

supporting

confidence: 79%

“…Next, we tested a number of organic Ca2" channel blockers for their ability to inhibit Mg2" refill in magnesium-depleted cells (17)(18)(19). Nifedipine, a 1,4 dihydropyridine derivative, inhibited the Mg2" influx pathway ( Figure 3.…”

mentioning

confidence: 99%

“…These results suggest that protein synthesis is partially involved with the adaptation of transport sites in cTAL cells after placement in magnesium-free media. Mg2+ influx was determined in magnesium-depleted cells as illus- (17)(18)(19)44). It should also be noted that Mg2" does not share the Ca2" channel in cardiac or vascular smooth muscle cells (reviewed in reference 44).…”

mentioning

confidence: 99%

“…These drugs appear to act at different sites along the length ofthe variously described Ca2+ channels particularly the L-type channels (17)(18)(19). It would appear that these sites are also common to the Mg2" pathways.…”

mentioning

confidence: 99%

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Intracellular Mg2+ and magnesium depletion in isolated renal thick ascending limb cells.

Quamme¹

1991

J. Clin. Invest.

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IntroductionMagnesium reabsorption and regulation within the kidney occur principally within the cortical thick ascending limb (cTAL) cells of the loop of Henle. Fluorometry with the dye, mag-fura- Homeostasis of total body magnesium occurs principally within the kidney by epithelial cells of the cortical segment of the thick ascending limb (cTAL)' of Henle's loop (1-3). Shareghi and Agus (4), using in vitro perfused tubules, provided evidence for passive magnesium transport probably moving through the paracellular pathway. These early observations were supported by the findings ofde Rouffignac and colleagues (1, 5). However, the later investigators also showed that magnesium transport may be altered in the absence of voltage and resistance changes and NaCl absorption, suggesting that magnesium transport may be active in nature (5).Although we have considerable understanding of transepithelial magnesium movement and some ofthe factors that control transport, little is known about the intracellular regulation ofmagnesium (1-5). This, has been due in part to the lack ofan adequate radiotracer of magnesium or other suitable quantitative methods (2, 6). More important was the deficiency of an adequate means of assessing free Mg2" activity. The recent development of fluorescent dyes for Mg2" should allow a better understanding of cellular free Mg2" movements (7). It is the free Mg2" concentration ([Mg2J]i) that is thought to be important in determining plasma membrane transport and entry into biochemical processes rather than total magnesium, much of which is bound to intracellular ligands (6).

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confidence: 79%

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confidence: 99%

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confidence: 99%

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Intracellular Mg2+ and magnesium depletion in isolated renal thick ascending limb cells.

Quamme¹

1991

J. Clin. Invest.

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“…It is now accepted that L-types in other tissues (133 -135), as well as other types in neurons (136)(137)(138)(139)(140)(141)(142)(143)(144), exist as a similar but distinct complex of subunits. N-type channels composed of a1-, a2-, 3-subunits are associated with the Go a-subunit, a 95-or 110-kDa protein, as well as syntaxin and synaptotagmin, that may be involved in neurotransmitter release (139,(142)(143)(144)(145).…”

Section: W-conotoxins and W-agatoxinsmentioning

confidence: 99%

Molecular Pharmacology of Voltage-Dependent Calcium Channels

Mori

Mikala

Váradi

et al. 1996

Japanese Journal of Pharmacology

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Antagonist binding sites of voltage-dependent calcium channels

Zamponi

1997

Drug Dev. Res.

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Voltage‐dependent calcium channels are crucial targets for a wide range of clinically active small organic pharmacological agents. These agents fall into several distinct classes of blockers, each associated with a unique site on the calcium channel α1 subunit. In addition, a number of peptide toxins isolated from invertebrates specifically bind to and block certain subtypes of voltage‐dependent calcium channels. Voltage‐dependent calcium channels are comprised of multiple subtypes, and not each of those subtypes are equally sensitive to small organic compounds and peptide blockers. Here, I present an overview of the classes of calcium channel blockers and our current understanding of their sites of action on the calcium channel protein. Drug Dev. Res. 42:131–143, 1997. © 1997 Wiley‐Liss, Inc.

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Molecular properties of calcium channels

Cited by 186 publications

References 292 publications

Intracellular Mg2+ and magnesium depletion in isolated renal thick ascending limb cells.

Intracellular Mg2+ and magnesium depletion in isolated renal thick ascending limb cells.

Molecular Pharmacology of Voltage-Dependent Calcium Channels

Antagonist binding sites of voltage-dependent calcium channels

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