In:
Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 95, No. 11 ( 1997-06-03), p. 2567-2572
Abstract:
Background Agonist-induced Ca 2+ entry is thought to be mediated by capacitative Ca 2+ entry other than L-type Ca 2+ channels in vascular smooth muscle cells (VSMCs). The mechanism for capacitative Ca 2+ entry has not been fully elucidated. Our objective was to examine the effect of external Mg 2+ on capacitative Ca 2+ entry in cultured rat aortic VSMCs. Methods and Results Three doses of external Mg 2+ concentration (nominally 0, 1, and 5 mmol/L) were used. After exposure to 1 μmol/L angiotensin II (Ang II) in Ca 2+ -free medium, addition of Ca 2+ to the medium caused an increase in cytosolic free Ca 2+ concentration ([Ca 2+ ] i ), indicating Ang II–induced Ca 2+ influx. This Ca 2+ influx was attenuated in cells preincubated with high external Mg 2+ concentrations or with 1 μmol/L nifedipine. After VSMCs in Ca 2+ -free medium were exposed to 1 μmol/L thapsigargin, which inhibits the sarcoplasmic reticulum Ca 2+ -ATPase and depletes Ca 2+ stores, addition of Ca 2+ to the medium induced an increase in [Ca 2+ ] i , indicating capacitative Ca 2+ entry. This entry pathway was found to be independent of dihydropyridine-sensitive Ca 2+ channels and inhibited by increased external Mg 2+ concentration. External Mg 2+ concentration did not influence Ca 2+ efflux across the plasma membrane after stimulation with Ang II plus thapsigargin. Conclusions Results suggest that in VSMCs, capacitative Ca 2+ entry is reduced by external Mg 2+ . This mechanism may explain in part the inhibitory effect of external Mg 2+ on Ca 2+ handling.
Type of Medium:
Online Resource
ISSN:
0009-7322
,
1524-4539
DOI:
10.1161/01.CIR.95.11.2567
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
1997
detail.hit.zdb_id:
1466401-X
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