<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Morel, Jean-Luc</dc:creator>
  <dc:creator>Dabertrand, Fabrice</dc:creator>
  <dc:creator>Porte, Yves</dc:creator>
  <dc:creator>Prévot, Anne</dc:creator>
  <dc:creator>Macrez, Nathalie</dc:creator>
  <dc:date>2014-08-01</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Microgravity induces a redistribution of blood volume. Consequently, astronauts' body  pressure is modified so that the upright blood pressure gradient is abolished, thereby  inducing a modification in cerebral blood pressure. This effect is mimicked in the  hindlimb unloaded rat model. After a duration of 8 days of unloading, Ca²⁺ signals  activated by depolarization and inositol-1,4,5-trisphosphate intracellular release were  increased in cerebral arteries. In the presence of ryanodine and thapsigargin, the  depolarization-induced Ca²⁺ signals remained increased in hindlimb suspended  animals, indicating that Ca²⁺ influx and Ca²⁺-induced Ca²⁺ release mechanism were  both increased. Spontaneous Ca²⁺ waves and localized Ca²⁺ events were also  investigated. Increases in both amplitude and frequency of spontaneous Ca²⁺ waves  were measured in hindlimb suspension conditions. After pharmacological segregation  of Ca²⁺ sparks and Ca²⁺ sparklets, their kinetic parameters were characterized.  Hindlimb suspension induced an increase in the frequencies of both Ca²⁺ localized  events, suggesting an increase of excitability. Labeling with bodipy compounds  suggested that voltage-dependent Ca²⁺ channels and ryanodine receptor expressions  were increased. Finally, the expression of the ryanodine receptor subtype 1 (RyR1)  was increased in hindlimb unloading conditions. Taken together, these results suggest  that RyR1 expression and voltage-dependent Ca²⁺ channels activity are the focal  points of the regulation of Ca²⁺ signals activated by vasoconstriction in rat cerebral  arteries with an increase of the voltage-dependent Ca²⁺ influx.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/303701</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/303701/files/pre_urr.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1007/s00424-013-1387-9</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Pflügers Archiv - European Journal of Physiology. - 2014, vol. 466, no. 8, p. 1517–1528</dc:source>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns1="xml" ns1:lang="en">Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
