ISSN:
1432-2013
Keywords:
Key words L-type Ca channel
;
Magnesium
;
Calcium
;
Ca channel potentiation
;
Na
;
Ca exchange
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract The effects of changing the intracellular concentrations of Ca2+ or Mg2+ ([Ca2+]i, [Mg2+]i) on Ca current (I Ca) was studied in frog ventricular myocytes using the whole-cell and cell-attached patch clamp techniques. In the physiological range of [Mg2+]i an increase in [Ca2+]i enhanced I Ca whereas at lower [Mg2+]i I Ca was suppressed. The increase in I Ca caused by Ca2+ loading was not mediated by phosphorylation since the kinase inhibitors H-8 {N-[2-(methylamino)-ethyl]-5-isoquinolinesulphonamide dihydrochloride}, staurosporine and KN-62 {1-[N,O-bis(5-isoquinolinesulphonyl)-N-methyl-1-tyrosyl]-4-phenylpiperazine} and a non-hydrolysable adenosine 5′-triphosphate analogue β,γ-methyleneadenosine 5′-triphosphate did not prevent the Ca2+-induced I Ca increase. I Ca was dramatically increased from 10 ± 6 (n = 4) to 71 ± 7 nA/nF (n = 4) when [Mg2+]i was lowered from 1.0 × 10−3 to 1.0 × 10−6 M at a [Ca2+]i of 10−8 M. The concentration response relation for inhibition of Ca channels by [Mg2+]i is modulated by [Ca2+]i. To account for the experimental results it is postulated that competitive binding of Ca2+ or Mg2+ to the Ca channel accelerates the transition of the channel from an active to a silent mode. Single-channel recordings support this hypothesis. The regulation may have clinical relevance in cytoprotection during cardiac ischaemia.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF02207267
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