<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>Leonard, Allison M.</dc:creator>
  <dc:creator>Chafe, Linda L.</dc:creator>
  <dc:creator>Montani, Jean-Pierre</dc:creator>
  <dc:creator>Vliet, Bruce N. Van</dc:creator>
  <dc:date>2006-12-08</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Background Although impaired nitric oxide production contributes importantly to salt- sensitivity, the role of the endothelial isoform of nitric oxide synthase (eNOS) has  received little attention. In the present study we compared the effects of a high-salt  diet on the blood pressure response of eNOS knockout (eNOS−/−) and control  (eNOS+/+) mice. Methods Mean arterial pressure (MAP), heart rate, pulse pressure,  and activity levels were recorded by telemetry in mice fed a regular-salt diet (0.7%  NaCl) followed by 6 weeks on either a high-salt (8% NaCl) or regular-salt diet. Results  The eNOS−/− mice exhibited a 15% increase in MAP and a 2- to 2.5-fold increase in  salt-sensitivity relative to the control strain. Salt-induced increases in MAP were well  sustained in eNOS−/−, whereas in eNOS+/+ the initial increase was biphasic. The  effects of salt on MAP were particularly pronounced during locomotor activity, during  the dark phase, and at the peak levels of MAP recorded over the course of the day.  The high-salt diet also led to a transient increase in the proportion of time spent  active. Levels of heart rate and pulse pressure were relatively unaffected by the high- salt diet. Conclusion The eNOS−/− mice exhibit an increased blood pressure  response to a high-salt diet. This finding suggests that eNOS normally provides an  important contribution to the body’s adaptation to a salt load and that reduced  production of NO by eNOS may promote salt-sensitivity and salt-induced  hypertension.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/300275</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/300275/files/19_12_1264.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.amjhyper.2006.05.025</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>American Journal of Hypertension. - 2006, vol. 19, no. 12, p. 1264-1269</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Sodium-dependent hypertension</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">mice</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">nitric oxide</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">nitric oxide synthase</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">blood pressure</dc:subject>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns6="xml" ns6:lang="en">Increased salt-sensitivity in endothelial nitric oxide synthase–knockout mice</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
