Exogenous and endogenous angiotensin‐II decrease renal cortical oxygen tension in conscious rats by limiting renal blood flow
Key points Our understanding of the mechanisms underlying the role of hypoxia in the initiation and progression of renal disease remains rudimentary. We have developed a method that allows wireless measurement of renal tissue oxygen tension in unrestrained rats. This method provides stable and conti...
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| Veröffentlicht in: | The Journal of physiology 2016-11, Vol.594 (21), p.6287-6300 |
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| creator | Emans, Tonja W. Janssen, Ben J. Pinkham, Maximilian I. Ow, Connie P. C. Evans, Roger G. Joles, Jaap A. Malpas, Simon C. Krediet, C. T. Paul Koeners, Maarten P. |
| description | Key points
Our understanding of the mechanisms underlying the role of hypoxia in the initiation and progression of renal disease remains rudimentary.
We have developed a method that allows wireless measurement of renal tissue oxygen tension in unrestrained rats.
This method provides stable and continuous measurements of cortical tissue oxygen tension (PO2) for more than 2 weeks and can reproducibly detect acute changes in cortical oxygenation.
Exogenous angiotensin‐II reduced renal cortical tissue PO2 more than equi‐pressor doses of phenylephrine, probably because it reduced renal oxygen delivery more than did phenylephrine.
Activation of the endogenous renin–angiotensin system in transgenic Cyp1a1Ren2 rats reduced cortical tissue PO2; in this model renal hypoxia precedes the development of structural pathology and can be reversed acutely by an angiotensin‐II receptor type 1 antagonist.
Angiotensin‐II promotes renal hypoxia, which may in turn contribute to its pathological effects during development of chronic kidney disease.
We hypothesised that both exogenous and endogenous angiotensin‐II (AngII) can decrease the partial pressure of oxygen (PO2) in the renal cortex of unrestrained rats, which might in turn contribute to the progression of chronic kidney disease. Rats were instrumented with telemeters equipped with a carbon paste electrode for continuous measurement of renal cortical tissue PO2. The method reproducibly detected acute changes in cortical oxygenation induced by systemic hyperoxia and hypoxia. In conscious rats, renal cortical PO2 was dose‐dependently reduced by intravenous AngII. Reductions in PO2 were significantly greater than those induced by equi‐pressor doses of phenylephrine. In anaesthetised rats, renal oxygen consumption was not affected, and filtration fraction was increased only in the AngII infused animals. Oxygen delivery decreased by 50% after infusion of AngII and renal blood flow (RBF) fell by 3.3 ml min−1. Equi‐pressor infusion of phenylephrine did not significantly reduce RBF or renal oxygen delivery. Activation of the endogenous renin–angiotensin system in Cyp1a1Ren2 transgenic rats reduced cortical tissue PO2. This could be reversed within minutes by pharmacological angiotensin‐II receptor type 1 (AT1R) blockade. Thus AngII is an important modulator of renal cortical oxygenation via AT1 receptors. AngII had a greater influence on cortical oxygenation than did phenylephrine. This phenomenon appears to be attributable to th |
| doi_str_mv | 10.1113/JP270731 |
| format | Article |
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Our understanding of the mechanisms underlying the role of hypoxia in the initiation and progression of renal disease remains rudimentary.
We have developed a method that allows wireless measurement of renal tissue oxygen tension in unrestrained rats.
This method provides stable and continuous measurements of cortical tissue oxygen tension (PO2) for more than 2 weeks and can reproducibly detect acute changes in cortical oxygenation.
Exogenous angiotensin‐II reduced renal cortical tissue PO2 more than equi‐pressor doses of phenylephrine, probably because it reduced renal oxygen delivery more than did phenylephrine.
Activation of the endogenous renin–angiotensin system in transgenic Cyp1a1Ren2 rats reduced cortical tissue PO2; in this model renal hypoxia precedes the development of structural pathology and can be reversed acutely by an angiotensin‐II receptor type 1 antagonist.
Angiotensin‐II promotes renal hypoxia, which may in turn contribute to its pathological effects during development of chronic kidney disease.
We hypothesised that both exogenous and endogenous angiotensin‐II (AngII) can decrease the partial pressure of oxygen (PO2) in the renal cortex of unrestrained rats, which might in turn contribute to the progression of chronic kidney disease. Rats were instrumented with telemeters equipped with a carbon paste electrode for continuous measurement of renal cortical tissue PO2. The method reproducibly detected acute changes in cortical oxygenation induced by systemic hyperoxia and hypoxia. In conscious rats, renal cortical PO2 was dose‐dependently reduced by intravenous AngII. Reductions in PO2 were significantly greater than those induced by equi‐pressor doses of phenylephrine. In anaesthetised rats, renal oxygen consumption was not affected, and filtration fraction was increased only in the AngII infused animals. Oxygen delivery decreased by 50% after infusion of AngII and renal blood flow (RBF) fell by 3.3 ml min−1. Equi‐pressor infusion of phenylephrine did not significantly reduce RBF or renal oxygen delivery. Activation of the endogenous renin–angiotensin system in Cyp1a1Ren2 transgenic rats reduced cortical tissue PO2. This could be reversed within minutes by pharmacological angiotensin‐II receptor type 1 (AT1R) blockade. Thus AngII is an important modulator of renal cortical oxygenation via AT1 receptors. AngII had a greater influence on cortical oxygenation than did phenylephrine. This phenomenon appears to be attributable to the profound impact of AngII on renal oxygen delivery. We conclude that the ability of AngII to promote renal cortical hypoxia may contribute to its influence on initiation and progression of chronic kidney disease.
Key points
Our understanding of the mechanisms underlying the role of hypoxia in the initiation and progression of renal disease remains rudimentary.
We have developed a method that allows wireless measurement of renal tissue oxygen tension in unrestrained rats.
This method provides stable and continuous measurements of cortical tissue oxygen tension (PO2) for more than 2 weeks and can reproducibly detect acute changes in cortical oxygenation.
Exogenous angiotensin‐II reduced renal cortical tissue PO2 more than equi‐pressor doses of phenylephrine, probably because it reduced renal oxygen delivery more than did phenylephrine.
Activation of the endogenous renin–angiotensin system in transgenic Cyp1a1Ren2 rats reduced cortical tissue PO2; in this model renal hypoxia precedes the development of structural pathology and can be reversed acutely by an angiotensin‐II receptor type 1 antagonist.
Angiotensin‐II promotes renal hypoxia, which may in turn contribute to its pathological effects during development of chronic kidney disease.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/JP270731</identifier><identifier>PMID: 27426098</identifier><identifier>CODEN: JPHYA7</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Angiotensin II - blood ; Angiotensin Receptor Antagonists - pharmacology ; angiotensin‐II ; Animals ; Consciousness ; cortex ; Cyp1a1Ren2 transgenic rat ; Cytochrome P-450 CYP1A1 - genetics ; hypoxia ; kidney ; Kidney - blood supply ; Kidney - drug effects ; Kidney - metabolism ; Kidney - physiology ; Male ; Oxygen Consumption ; oxygenation ; phenylephrine ; Phenylephrine - pharmacology ; Rats ; Rats, Wistar ; Renal and Endocrine ; Renal Circulation ; Renin - genetics ; Renin-Angiotensin System ; Research Paper ; telemetry ; Vasoconstrictor Agents - pharmacology</subject><ispartof>The Journal of physiology, 2016-11, Vol.594 (21), p.6287-6300</ispartof><rights>2016 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society</rights><rights>2016 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.</rights><rights>Journal compilation © 2016 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5376-d72af3c20534461f321c1c18eca0cbc755ceb8cc898410bd3afba81e1a9b10c43</citedby><cites>FETCH-LOGICAL-c5376-d72af3c20534461f321c1c18eca0cbc755ceb8cc898410bd3afba81e1a9b10c43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5088249/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5088249/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,1418,1434,27929,27930,45579,45580,46414,46838,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27426098$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Emans, Tonja W.</creatorcontrib><creatorcontrib>Janssen, Ben J.</creatorcontrib><creatorcontrib>Pinkham, Maximilian I.</creatorcontrib><creatorcontrib>Ow, Connie P. C.</creatorcontrib><creatorcontrib>Evans, Roger G.</creatorcontrib><creatorcontrib>Joles, Jaap A.</creatorcontrib><creatorcontrib>Malpas, Simon C.</creatorcontrib><creatorcontrib>Krediet, C. T. Paul</creatorcontrib><creatorcontrib>Koeners, Maarten P.</creatorcontrib><title>Exogenous and endogenous angiotensin‐II decrease renal cortical oxygen tension in conscious rats by limiting renal blood flow</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Key points
Our understanding of the mechanisms underlying the role of hypoxia in the initiation and progression of renal disease remains rudimentary.
We have developed a method that allows wireless measurement of renal tissue oxygen tension in unrestrained rats.
This method provides stable and continuous measurements of cortical tissue oxygen tension (PO2) for more than 2 weeks and can reproducibly detect acute changes in cortical oxygenation.
Exogenous angiotensin‐II reduced renal cortical tissue PO2 more than equi‐pressor doses of phenylephrine, probably because it reduced renal oxygen delivery more than did phenylephrine.
Activation of the endogenous renin–angiotensin system in transgenic Cyp1a1Ren2 rats reduced cortical tissue PO2; in this model renal hypoxia precedes the development of structural pathology and can be reversed acutely by an angiotensin‐II receptor type 1 antagonist.
Angiotensin‐II promotes renal hypoxia, which may in turn contribute to its pathological effects during development of chronic kidney disease.
We hypothesised that both exogenous and endogenous angiotensin‐II (AngII) can decrease the partial pressure of oxygen (PO2) in the renal cortex of unrestrained rats, which might in turn contribute to the progression of chronic kidney disease. Rats were instrumented with telemeters equipped with a carbon paste electrode for continuous measurement of renal cortical tissue PO2. The method reproducibly detected acute changes in cortical oxygenation induced by systemic hyperoxia and hypoxia. In conscious rats, renal cortical PO2 was dose‐dependently reduced by intravenous AngII. Reductions in PO2 were significantly greater than those induced by equi‐pressor doses of phenylephrine. In anaesthetised rats, renal oxygen consumption was not affected, and filtration fraction was increased only in the AngII infused animals. Oxygen delivery decreased by 50% after infusion of AngII and renal blood flow (RBF) fell by 3.3 ml min−1. Equi‐pressor infusion of phenylephrine did not significantly reduce RBF or renal oxygen delivery. Activation of the endogenous renin–angiotensin system in Cyp1a1Ren2 transgenic rats reduced cortical tissue PO2. This could be reversed within minutes by pharmacological angiotensin‐II receptor type 1 (AT1R) blockade. Thus AngII is an important modulator of renal cortical oxygenation via AT1 receptors. AngII had a greater influence on cortical oxygenation than did phenylephrine. This phenomenon appears to be attributable to the profound impact of AngII on renal oxygen delivery. We conclude that the ability of AngII to promote renal cortical hypoxia may contribute to its influence on initiation and progression of chronic kidney disease.
Key points
Our understanding of the mechanisms underlying the role of hypoxia in the initiation and progression of renal disease remains rudimentary.
We have developed a method that allows wireless measurement of renal tissue oxygen tension in unrestrained rats.
This method provides stable and continuous measurements of cortical tissue oxygen tension (PO2) for more than 2 weeks and can reproducibly detect acute changes in cortical oxygenation.
Exogenous angiotensin‐II reduced renal cortical tissue PO2 more than equi‐pressor doses of phenylephrine, probably because it reduced renal oxygen delivery more than did phenylephrine.
Activation of the endogenous renin–angiotensin system in transgenic Cyp1a1Ren2 rats reduced cortical tissue PO2; in this model renal hypoxia precedes the development of structural pathology and can be reversed acutely by an angiotensin‐II receptor type 1 antagonist.
Angiotensin‐II promotes renal hypoxia, which may in turn contribute to its pathological effects during development of chronic kidney disease.</description><subject>Angiotensin II - blood</subject><subject>Angiotensin Receptor Antagonists - pharmacology</subject><subject>angiotensin‐II</subject><subject>Animals</subject><subject>Consciousness</subject><subject>cortex</subject><subject>Cyp1a1Ren2 transgenic rat</subject><subject>Cytochrome P-450 CYP1A1 - genetics</subject><subject>hypoxia</subject><subject>kidney</subject><subject>Kidney - blood supply</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - physiology</subject><subject>Male</subject><subject>Oxygen Consumption</subject><subject>oxygenation</subject><subject>phenylephrine</subject><subject>Phenylephrine - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Renal and Endocrine</subject><subject>Renal Circulation</subject><subject>Renin - genetics</subject><subject>Renin-Angiotensin System</subject><subject>Research Paper</subject><subject>telemetry</subject><subject>Vasoconstrictor Agents - pharmacology</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp1kd9qFDEYxYMo7boWfAIJeOPNaP7NJLkRpFTdUmgv6nXIZL5ZU7JJTWZt90ofwWf0Scy22z8KkoskfL9zOB8HoZeUvKWU8nfHZ0wSyekTNKOi042Umj9FM0IYa7hs6T56XsoFIZQTrffQPpOCdUSrGfpxdJ2WENO6YBsHDHF4-C59miAWH3___LVY4AFcBlsAZ4g2YJfy5F19pOtNleAbNEXsYx3F4vzWJNup4H6Dg1_5ycflTtuHlAY8hnT1Aj0bbShwsLvn6MvHo_PDz83J6afF4YeTxrVcds0gmR25Y6TlQnR05Iy6ehQ4S1zvZNs66JVzSitBST9wO_ZWUaBW95Q4wefo_a3v5bpfweAgTtkGc5n9yuaNSdabvyfRfzXL9N20RCkmdDV4szPI6dsaymRWvjgIwUaomxqqeC1A8Zpwjl7_g16kda5731CCirbT8sHQ5VRKhvE-DCVm26q5a7Wirx6HvwfvaqxAcwtc-QCb_xqZ8-OzrYT_AZ9Trlw</recordid><startdate>20161101</startdate><enddate>20161101</enddate><creator>Emans, Tonja W.</creator><creator>Janssen, Ben J.</creator><creator>Pinkham, Maximilian I.</creator><creator>Ow, Connie P. C.</creator><creator>Evans, Roger G.</creator><creator>Joles, Jaap A.</creator><creator>Malpas, Simon C.</creator><creator>Krediet, C. T. Paul</creator><creator>Koeners, Maarten P.</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>20161101</creationdate><title>Exogenous and endogenous angiotensin‐II decrease renal cortical oxygen tension in conscious rats by limiting renal blood flow</title><author>Emans, Tonja W. ; Janssen, Ben J. ; Pinkham, Maximilian I. ; Ow, Connie P. C. ; Evans, Roger G. ; Joles, Jaap A. ; Malpas, Simon C. ; Krediet, C. T. Paul ; Koeners, Maarten P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5376-d72af3c20534461f321c1c18eca0cbc755ceb8cc898410bd3afba81e1a9b10c43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Angiotensin II - blood</topic><topic>Angiotensin Receptor Antagonists - pharmacology</topic><topic>angiotensin‐II</topic><topic>Animals</topic><topic>Consciousness</topic><topic>cortex</topic><topic>Cyp1a1Ren2 transgenic rat</topic><topic>Cytochrome P-450 CYP1A1 - genetics</topic><topic>hypoxia</topic><topic>kidney</topic><topic>Kidney - blood supply</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - physiology</topic><topic>Male</topic><topic>Oxygen Consumption</topic><topic>oxygenation</topic><topic>phenylephrine</topic><topic>Phenylephrine - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Renal and Endocrine</topic><topic>Renal Circulation</topic><topic>Renin - genetics</topic><topic>Renin-Angiotensin System</topic><topic>Research Paper</topic><topic>telemetry</topic><topic>Vasoconstrictor Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Emans, Tonja W.</creatorcontrib><creatorcontrib>Janssen, Ben J.</creatorcontrib><creatorcontrib>Pinkham, Maximilian I.</creatorcontrib><creatorcontrib>Ow, Connie P. C.</creatorcontrib><creatorcontrib>Evans, Roger G.</creatorcontrib><creatorcontrib>Joles, Jaap A.</creatorcontrib><creatorcontrib>Malpas, Simon C.</creatorcontrib><creatorcontrib>Krediet, C. T. Paul</creatorcontrib><creatorcontrib>Koeners, Maarten P.</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Emans, Tonja W.</au><au>Janssen, Ben J.</au><au>Pinkham, Maximilian I.</au><au>Ow, Connie P. C.</au><au>Evans, Roger G.</au><au>Joles, Jaap A.</au><au>Malpas, Simon C.</au><au>Krediet, C. T. Paul</au><au>Koeners, Maarten P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exogenous and endogenous angiotensin‐II decrease renal cortical oxygen tension in conscious rats by limiting renal blood flow</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2016-11-01</date><risdate>2016</risdate><volume>594</volume><issue>21</issue><spage>6287</spage><epage>6300</epage><pages>6287-6300</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><coden>JPHYA7</coden><abstract>Key points
Our understanding of the mechanisms underlying the role of hypoxia in the initiation and progression of renal disease remains rudimentary.
We have developed a method that allows wireless measurement of renal tissue oxygen tension in unrestrained rats.
This method provides stable and continuous measurements of cortical tissue oxygen tension (PO2) for more than 2 weeks and can reproducibly detect acute changes in cortical oxygenation.
Exogenous angiotensin‐II reduced renal cortical tissue PO2 more than equi‐pressor doses of phenylephrine, probably because it reduced renal oxygen delivery more than did phenylephrine.
Activation of the endogenous renin–angiotensin system in transgenic Cyp1a1Ren2 rats reduced cortical tissue PO2; in this model renal hypoxia precedes the development of structural pathology and can be reversed acutely by an angiotensin‐II receptor type 1 antagonist.
Angiotensin‐II promotes renal hypoxia, which may in turn contribute to its pathological effects during development of chronic kidney disease.
We hypothesised that both exogenous and endogenous angiotensin‐II (AngII) can decrease the partial pressure of oxygen (PO2) in the renal cortex of unrestrained rats, which might in turn contribute to the progression of chronic kidney disease. Rats were instrumented with telemeters equipped with a carbon paste electrode for continuous measurement of renal cortical tissue PO2. The method reproducibly detected acute changes in cortical oxygenation induced by systemic hyperoxia and hypoxia. In conscious rats, renal cortical PO2 was dose‐dependently reduced by intravenous AngII. Reductions in PO2 were significantly greater than those induced by equi‐pressor doses of phenylephrine. In anaesthetised rats, renal oxygen consumption was not affected, and filtration fraction was increased only in the AngII infused animals. Oxygen delivery decreased by 50% after infusion of AngII and renal blood flow (RBF) fell by 3.3 ml min−1. Equi‐pressor infusion of phenylephrine did not significantly reduce RBF or renal oxygen delivery. Activation of the endogenous renin–angiotensin system in Cyp1a1Ren2 transgenic rats reduced cortical tissue PO2. This could be reversed within minutes by pharmacological angiotensin‐II receptor type 1 (AT1R) blockade. Thus AngII is an important modulator of renal cortical oxygenation via AT1 receptors. AngII had a greater influence on cortical oxygenation than did phenylephrine. This phenomenon appears to be attributable to the profound impact of AngII on renal oxygen delivery. We conclude that the ability of AngII to promote renal cortical hypoxia may contribute to its influence on initiation and progression of chronic kidney disease.
Key points
Our understanding of the mechanisms underlying the role of hypoxia in the initiation and progression of renal disease remains rudimentary.
We have developed a method that allows wireless measurement of renal tissue oxygen tension in unrestrained rats.
This method provides stable and continuous measurements of cortical tissue oxygen tension (PO2) for more than 2 weeks and can reproducibly detect acute changes in cortical oxygenation.
Exogenous angiotensin‐II reduced renal cortical tissue PO2 more than equi‐pressor doses of phenylephrine, probably because it reduced renal oxygen delivery more than did phenylephrine.
Activation of the endogenous renin–angiotensin system in transgenic Cyp1a1Ren2 rats reduced cortical tissue PO2; in this model renal hypoxia precedes the development of structural pathology and can be reversed acutely by an angiotensin‐II receptor type 1 antagonist.
Angiotensin‐II promotes renal hypoxia, which may in turn contribute to its pathological effects during development of chronic kidney disease.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>27426098</pmid><doi>10.1113/JP270731</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| source | Wiley Online Library - AutoHoldings Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Angiotensin II - blood Angiotensin Receptor Antagonists - pharmacology angiotensin‐II Animals Consciousness cortex Cyp1a1Ren2 transgenic rat Cytochrome P-450 CYP1A1 - genetics hypoxia kidney Kidney - blood supply Kidney - drug effects Kidney - metabolism Kidney - physiology Male Oxygen Consumption oxygenation phenylephrine Phenylephrine - pharmacology Rats Rats, Wistar Renal and Endocrine Renal Circulation Renin - genetics Renin-Angiotensin System Research Paper telemetry Vasoconstrictor Agents - pharmacology |
| title | Exogenous and endogenous angiotensin‐II decrease renal cortical oxygen tension in conscious rats by limiting renal blood flow |
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