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Trans- and cis-resveratrol increase cytoplasmic calcium levels in A7r5 vascular smooth muscle cells

The effects of trans‐ and cis‐resveratrol on cytosolic Ca2+ concentration ([Ca2+]i) were studied using fura‐2 in vascular smooth muscle cells (A7r5). Both isomers of resveratrol caused a sustained elevation in [Ca2+]i, cis‐resveratrol being significantly more effective than the trans‐isomer. The res...

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Published in:Molecular nutrition & food research 2005-05, Vol.49 (5), p.396-404
Main Authors: Campos-Toimil, Manuel, Elíes, Jacobo, Orallo, Francisco
Format: Article
Language:English
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Summary:The effects of trans‐ and cis‐resveratrol on cytosolic Ca2+ concentration ([Ca2+]i) were studied using fura‐2 in vascular smooth muscle cells (A7r5). Both isomers of resveratrol caused a sustained elevation in [Ca2+]i, cis‐resveratrol being significantly more effective than the trans‐isomer. The resveratrol‐induced increase in [Ca2+]i was significantly potentiated by the previous application of low concentrations of thapsigargin, partially inhibited by nifedipine or Ni2+, and not affected by SKF 96365. In the absence of extracellular Ca2+, both isomers of resveratrol induced a transient, slow increase in [Ca2+]i, which was inhibited by the previous depletion of intracellular stores with thapsigargin and completely blocked by preincubation with TMB‐8, an inhibitor of intracellular calcium release. Reintroduction of Ca2+ in the external solution after the resveratrol‐induced release of Ca2+ activated the Ca2+ influx through store‐operated calcium channels. The resveratrol‐induced increase in [Ca2+]i in the absence of extracelullar Ca2+ partially reduced the increase in [Ca2+]i evoked by the subsequent application of thapsigargin. Our results suggest that trans‐ and cis‐resveratrol induce a depletion of Ca2+ from the same intracellular stores released by thapsigargin and subsequent capacitative influx of Ca2+. Additionally, a direct activation of transmembrane Ca2+ influx through another type of channel may be also implicated.
ISSN:1613-4125
1613-4133
DOI:10.1002/mnfr.200400108