<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>Huet F</dc:creator>
  <dc:creator>Gouyon JB</dc:creator>
  <dc:creator>Guignard JP</dc:creator>
  <dc:date>1997</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">The role of angiotensin II, a potent postglomerular vasoconstrictor, in the hypoxemia-induced renal changes is still controversial. The ability of perindoprilat, an angiotensin converting-enzyme inhibitor, to prevent the acute renal effects of hypoxemia was assessed in 22 anesthetized-ventilated rabbits. In 8 untreated rabbits, hypoxemia induced a significant drop in mean blood pressure (MBP) (-12 +/- 2%), glomerular filtration rate (GFR) (-16 +/- 3%) and renal blood flow (RBF) (-12 +/- 3%) with a concomittant increase in renal vascular resistance (RVR) (+18 +/- 5%) and urine flow rate (+33 +/- 14%), and without any changes in filtration fraction (FF) (-4 +/- 2%). This suggests the occurrence of glomerular vasoconstriction during the hypoxemic stress. In 7 normoxemic rabbits, intravenous perindoprilat (20 microg/kg) induced an increase in urine flow rate (+17 +/- 4%) and RBF (+17 +/- 4%), and a decrease in MBP (-6 +/- 1%), RVR (-14 +/- 3%) and FF (-11 +/- 2%) without a significant change in GFR. The drop in FF and the increase in RBF suggests preferential postglomerular vasodilatation. In 7 rabbits, perindoprilat prevented the occurence of the hypoxemia-induced changes in RBF and RVR without improving MBP. FF decreased significantly (-18 +/- 2%), while the drop in GFR (-7 +/- 2%) was partially blunted and the increase in urine flow rate (+25 +/- 9%) was confirmed. These results could be explained by the inhibition of the angiotensin-mediated efferent vasoconstriction and by the inhibition of bradykinin degradation by perindoprilat. These data confirm the ability of converting-enzyme inhibitors to prevent the renal hypoperfusion induced by acute hypoxemia.</dc:description>
  <dc:identifier>https://sonar.ch/global/documents/277735</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/s0024-3205(97)00918-1</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/9393935</dc:relation>
  <dc:source>Life sciences. - 1997</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Angiotensin II</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Angiotensin-Converting Enzyme Inhibitors</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Animals</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Blood Pressure</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Carbon Dioxide</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Glomerular Filtration Rate</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Hypoxia</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Indoles</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Kidney Diseases</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Oxygen</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">Partial Pressure</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">Rabbits</dc:subject>
  <dc:subject xmlns:ns13="xml" ns13:lang="en">Renal Circulation</dc:subject>
  <dc:subject xmlns:ns14="xml" ns14:lang="en">Vasoconstriction</dc:subject>
  <dc:title xmlns:ns15="xml" ns15:lang="en">Prevention of hypoxemia-induced renal dysfunction by perindoprilat in the rabbit.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>