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Chronic ACE inhibitor treatment increases angiotensin type 1 receptor binding in vivo in the dog kidney

Purpose PET imaging has been recently introduced for investigating the type 1 angiotensin II receptor (AT 1 R) in vivo . The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT 1 R in the dog kidney. Meth...

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Published in:European journal of nuclear medicine and molecular imaging 2008-06, Vol.35 (6), p.1109-1116
Main Authors: Zober, Tamas G., Fabucci, Maria Elena, Zheng, Wei, Brown, Phillip R., Seckin, Esen, Mathews, William B., Sandberg, Kathryn, Szabo, Zsolt
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cited_by cdi_FETCH-LOGICAL-c400t-a1c02fa1f469d304648c432668321610d19bb9fe4c466d5d0ddecc70910881833
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container_issue 6
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container_title European journal of nuclear medicine and molecular imaging
container_volume 35
creator Zober, Tamas G.
Fabucci, Maria Elena
Zheng, Wei
Brown, Phillip R.
Seckin, Esen
Mathews, William B.
Sandberg, Kathryn
Szabo, Zsolt
description Purpose PET imaging has been recently introduced for investigating the type 1 angiotensin II receptor (AT 1 R) in vivo . The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT 1 R in the dog kidney. Methods Animals were imaged at baseline, after acute intravenous ACEI treatment and after a chronic 2-week exposure to an oral ACEI. Control animals were imaged at identical time points in the absence of ACEI treatment. Results In vivo AT 1 R binding expressed by K i was increased in the renal cortex by chronic ACEI treatment ( p  
doi_str_mv 10.1007/s00259-007-0667-z
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The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT 1 R in the dog kidney. Methods Animals were imaged at baseline, after acute intravenous ACEI treatment and after a chronic 2-week exposure to an oral ACEI. Control animals were imaged at identical time points in the absence of ACEI treatment. Results In vivo AT 1 R binding expressed by K i was increased in the renal cortex by chronic ACEI treatment ( p  &lt; 0.05). In vitro measurements of AT 1 R density ( B max ) also revealed significant increases in AT 1 R in isolated glomeruli ( p  &lt; 0.05). Plasma renin activity was increased, but angiotensin II (Ang II) and the Ang II/Ang I ratio showed a weak correlation with chronic ACEI treatment, consistent with an Ang II escape phenomenon. Conclusion This study reveals, for the first time, that chronic ACEI treatment increases AT 1 R binding in vivo in the dog renal cortex.</description><identifier>ISSN: 1619-7070</identifier><identifier>EISSN: 1619-7089</identifier><identifier>DOI: 10.1007/s00259-007-0667-z</identifier><identifier>PMID: 18180920</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Angiotensin-Converting Enzyme Inhibitors - administration &amp; dosage ; Animals ; Binding sites ; Cardiology ; Dogs ; Dose-Response Relationship, Drug ; Enzymes ; Imaging ; Inhibitor drugs ; Kidney - diagnostic imaging ; Kidney - drug effects ; Kidney - metabolism ; Kidneys ; Male ; Medicine ; Medicine &amp; Public Health ; Nuclear Medicine ; Oncology ; Original Article ; Orthopedics ; Protein Binding - drug effects ; Radiology ; Radionuclide Imaging ; Receptor, Angiotensin, Type 1 - metabolism ; Tomography</subject><ispartof>European journal of nuclear medicine and molecular imaging, 2008-06, Vol.35 (6), p.1109-1116</ispartof><rights>Springer-Verlag 2007</rights><rights>Springer-Verlag 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c400t-a1c02fa1f469d304648c432668321610d19bb9fe4c466d5d0ddecc70910881833</citedby><cites>FETCH-LOGICAL-c400t-a1c02fa1f469d304648c432668321610d19bb9fe4c466d5d0ddecc70910881833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18180920$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zober, Tamas G.</creatorcontrib><creatorcontrib>Fabucci, Maria Elena</creatorcontrib><creatorcontrib>Zheng, Wei</creatorcontrib><creatorcontrib>Brown, Phillip R.</creatorcontrib><creatorcontrib>Seckin, Esen</creatorcontrib><creatorcontrib>Mathews, William B.</creatorcontrib><creatorcontrib>Sandberg, Kathryn</creatorcontrib><creatorcontrib>Szabo, Zsolt</creatorcontrib><title>Chronic ACE inhibitor treatment increases angiotensin type 1 receptor binding in vivo in the dog kidney</title><title>European journal of nuclear medicine and molecular imaging</title><addtitle>Eur J Nucl Med Mol Imaging</addtitle><addtitle>Eur J Nucl Med Mol Imaging</addtitle><description>Purpose PET imaging has been recently introduced for investigating the type 1 angiotensin II receptor (AT 1 R) in vivo . The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT 1 R in the dog kidney. Methods Animals were imaged at baseline, after acute intravenous ACEI treatment and after a chronic 2-week exposure to an oral ACEI. Control animals were imaged at identical time points in the absence of ACEI treatment. Results In vivo AT 1 R binding expressed by K i was increased in the renal cortex by chronic ACEI treatment ( p  &lt; 0.05). In vitro measurements of AT 1 R density ( B max ) also revealed significant increases in AT 1 R in isolated glomeruli ( p  &lt; 0.05). Plasma renin activity was increased, but angiotensin II (Ang II) and the Ang II/Ang I ratio showed a weak correlation with chronic ACEI treatment, consistent with an Ang II escape phenomenon. 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The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT 1 R in the dog kidney. Methods Animals were imaged at baseline, after acute intravenous ACEI treatment and after a chronic 2-week exposure to an oral ACEI. Control animals were imaged at identical time points in the absence of ACEI treatment. Results In vivo AT 1 R binding expressed by K i was increased in the renal cortex by chronic ACEI treatment ( p  &lt; 0.05). In vitro measurements of AT 1 R density ( B max ) also revealed significant increases in AT 1 R in isolated glomeruli ( p  &lt; 0.05). Plasma renin activity was increased, but angiotensin II (Ang II) and the Ang II/Ang I ratio showed a weak correlation with chronic ACEI treatment, consistent with an Ang II escape phenomenon. Conclusion This study reveals, for the first time, that chronic ACEI treatment increases AT 1 R binding in vivo in the dog renal cortex.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>18180920</pmid><doi>10.1007/s00259-007-0667-z</doi><tpages>8</tpages></addata></record>
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subjects Angiotensin-Converting Enzyme Inhibitors - administration & dosage
Animals
Binding sites
Cardiology
Dogs
Dose-Response Relationship, Drug
Enzymes
Imaging
Inhibitor drugs
Kidney - diagnostic imaging
Kidney - drug effects
Kidney - metabolism
Kidneys
Male
Medicine
Medicine & Public Health
Nuclear Medicine
Oncology
Original Article
Orthopedics
Protein Binding - drug effects
Radiology
Radionuclide Imaging
Receptor, Angiotensin, Type 1 - metabolism
Tomography
title Chronic ACE inhibitor treatment increases angiotensin type 1 receptor binding in vivo in the dog kidney
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