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Trans ‐ and cis ‐resveratrol increase cytoplasmic calcium levels in A7r5 vascular smooth muscle cells
Author(s) -
CamposToimil Manuel,
Elíes Jacobo,
Orallo Francisco
Publication year - 2005
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200400108
Subject(s) - thapsigargin , resveratrol , vascular smooth muscle , extracellular , intracellular , chemistry , calcium , nifedipine , cytosol , calcium in biology , fura 2 , biophysics , voltage dependent calcium channel , biochemistry , endocrinology , medicine , biology , smooth muscle , enzyme , organic chemistry
The effects of trans ‐ and cis ‐resveratrol on cytosolic Ca 2+ concentration ([Ca 2+ ] i ) were studied using fura‐2 in vascular smooth muscle cells (A7r5). Both isomers of resveratrol caused a sustained elevation in [Ca 2+ ] i , cis ‐resveratrol being significantly more effective than the trans‐ isomer. The resveratrol‐induced increase in [Ca 2+ ] i was significantly potentiated by the previous application of low concentrations of thapsigargin, partially inhibited by nifedipine or Ni 2+ , and not affected by SKF 96365. In the absence of extracellular Ca 2+ , both isomers of resveratrol induced a transient, slow increase in [Ca 2+ ] 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 Ca 2+ in the external solution after the resveratrol‐induced release of Ca 2+ activated the Ca 2+ influx through store‐operated calcium channels. The resveratrol‐induced increase in [Ca 2+ ] i in the absence of extracelullar Ca 2+ partially reduced the increase in [Ca 2+ ] i evoked by the subsequent application of thapsigargin. Our results suggest that trans ‐ and cis ‐resveratrol induce a depletion of Ca 2+ from the same intracellular stores released by thapsigargin and subsequent capacitative influx of Ca 2+ . Additionally, a direct activation of transmembrane Ca 2+ influx through another type of channel may be also implicated.