<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>Eisele, Nicole</dc:creator>
  <dc:creator>Klossner, Rahel</dc:creator>
  <dc:creator>Escher, Geneviève</dc:creator>
  <dc:creator>Rudloff, Stefan</dc:creator>
  <dc:creator>Larionov, Alexey</dc:creator>
  <dc:creator>Theilig, Franziska</dc:creator>
  <dc:creator>Mohaupt, Markus G.</dc:creator>
  <dc:creator>Mistry, Hiten D.</dc:creator>
  <dc:creator>Gennari‐Moser, Carine</dc:creator>
  <dc:date>2018-08-07</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">In pregnancy, a high plasma volume maintains uteroplacental perfusion and prevents  placental ischemia, a condition linked to elevated maternal blood pressure (BP).  Reducing BP by increasing Na+ intake via plasma volume expansion appears contra‐ intuitive. We hypothesize that an appropriate Na+ intake in pregnancy reduces  maternal BP and adapts the renin‐angiotensin system in a pregnancy‐specific  manner.Methods and Results: BP was measured by implanted telemetry in Sprague‐ Dawley rats before and throughout pregnancy. Pregnant and nonpregnant animals  received either a normal‐salt (0.4%; NS), high‐salt (8%; HS), or low‐salt (0.01%; LS)  diet, or HS (days 1–14) followed by LS (days 14–20) diet (HS/LS). Before delivery  (day 20), animals were euthanized and organs collected. Food, water, and Na+ intake  were monitored in metabolic cages, and urinary creatinine and Na+ were analyzed.  Na+ intake and retention increased in pregnancy (NS, LS), leading to a positive Na+  balance (NS, LS). BP was stable during LS, but reduced in HS conditions in  pregnancy. The renin‐angiotensin system was adapted as expected. Activating  cleavage of α‐ and γ‐subunits of the renal epithelial Na+ channel and expression of‐ full length medullary β‐subunits, accentuated further in all LS conditions, were  upregulated in pregnancy.Conclusions: Pregnancy led to Na+ retention adapted to  dietary changes. HS exposure paradoxically reduced BP. Na+ uptake while only  modestly linked to the renin‐angiotensin system is enhanced in the presence of  posttranslational renal epithelial Na+ channel modifications. This suggests (1) storage  of Na+ in pregnancy upon HS exposure, bridging periods of LS availability; and (2)  that potentially non–renin‐angiotensin–related mechanisms participate in ENaC  activation and consecutive Na+ retention.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/307281</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/307281/files/lar_pmr.pdf</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/307281/files/lar_pmr_sm.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1161/JAHA.117.008363</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Journal of the American Heart Association. - 2018, vol. 7, no. 15, p. e008363</dc:source>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns1="xml" ns1:lang="en">Physiological and Molecular Responses to Altered Sodium Intake in Rat Pregnancy</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
