Role of endothelin ET(A) receptor antagonism in the post-transplant renal response to angiotensin II in the rat
The role of endothelins in the renal damage associated with ischaemic-reperfusion (I-R) injury during organ transplantation was determined by selective blockade of the ET(A) receptors with the receptor antagonist ABT-627. The integrity of kidney function was determined 2 and 8 weeks after transplant...
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| Veröffentlicht in: | Experimental physiology 2001-05, Vol.86 (3), p.365-372 |
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| creator | Hammad, F T Wheatley, A M Davis, G |
| description | The role of endothelins in the renal damage associated with ischaemic-reperfusion (I-R) injury during organ transplantation
was determined by selective blockade of the ET(A) receptors with the receptor antagonist ABT-627. The integrity of kidney
function was determined 2 and 8 weeks after transplantation by investigation of the renal response to angiotensin II. Under
pentobarbitone anaesthesia (70 mg x kg(-1), I.P.), rats underwent a right nephrectomy. Transplantation of the left kidney
was performed after 2 h cold ischaemia without or with ABT-627 treatment. Control animals underwent left renal denervation.
The renal response to angiotensin II was measured 2 weeks later following blockade of endogenous production of angiotensin
II with captopril. A further transplant group was allowed to recover for 8 weeks before the terminal study. In the control
group, angiotensin II reduced renal blood flow (RBF), glomerular filtration rate (GFR), urine flow rate (UV), and fractional
sodium excretion (FE(Na)) by 29 +/- 5 %, 19 +/- 4 %, 25 +/- 4 % and 32 +/- 7 %, respectively. Conversely, in the transplant
group, angiotensin II left RBF unchanged and increased GFR (59 +/- 12 %) and UV (93 +/- 8 %). FE(Na) decreased by 24 +/- 9
%. In both the transplant group treated with ABT-627 and the long-term recovery group, the renal response to angiotensin II
was normalised. In conclusion, renal transplantation following 2 h cold I-R injury resulted in a temporary abnormal renal
response to angiotensin II, which was reversed by ET(A) receptor antagonism at the time of transplantation. |
| doi_str_mv | 10.1113/eph8602137 |
| format | Article |
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was determined by selective blockade of the ET(A) receptors with the receptor antagonist ABT-627. The integrity of kidney
function was determined 2 and 8 weeks after transplantation by investigation of the renal response to angiotensin II. Under
pentobarbitone anaesthesia (70 mg x kg(-1), I.P.), rats underwent a right nephrectomy. Transplantation of the left kidney
was performed after 2 h cold ischaemia without or with ABT-627 treatment. Control animals underwent left renal denervation.
The renal response to angiotensin II was measured 2 weeks later following blockade of endogenous production of angiotensin
II with captopril. A further transplant group was allowed to recover for 8 weeks before the terminal study. In the control
group, angiotensin II reduced renal blood flow (RBF), glomerular filtration rate (GFR), urine flow rate (UV), and fractional
sodium excretion (FE(Na)) by 29 +/- 5 %, 19 +/- 4 %, 25 +/- 4 % and 32 +/- 7 %, respectively. Conversely, in the transplant
group, angiotensin II left RBF unchanged and increased GFR (59 +/- 12 %) and UV (93 +/- 8 %). FE(Na) decreased by 24 +/- 9
%. In both the transplant group treated with ABT-627 and the long-term recovery group, the renal response to angiotensin II
was normalised. In conclusion, renal transplantation following 2 h cold I-R injury resulted in a temporary abnormal renal
response to angiotensin II, which was reversed by ET(A) receptor antagonism at the time of transplantation.</description><identifier>ISSN: 0958-0670</identifier><identifier>EISSN: 1469-445X</identifier><identifier>DOI: 10.1113/eph8602137</identifier><identifier>PMID: 11429654</identifier><language>eng</language><publisher>England: The Physiological Society</publisher><subject>Angiotensin II - antagonists & inhibitors ; Angiotensin II - metabolism ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Animals ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Captopril - pharmacology ; Cold Temperature ; Endothelin Receptor Antagonists ; Glomerular Filtration Rate - drug effects ; Glomerular Filtration Rate - physiology ; Ischemia - physiopathology ; Kidney Transplantation ; Male ; Pyrrolidines - pharmacology ; Rats ; Rats, Inbred Lew ; Receptor, Endothelin A ; Renal Circulation - drug effects ; Renal Circulation - physiology ; Renin-Angiotensin System - drug effects ; Renin-Angiotensin System - physiology ; Sodium - urine</subject><ispartof>Experimental physiology, 2001-05, Vol.86 (3), p.365-372</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1614-c5d7c9dbd2229de6ceaeb56b5c2707cb96afa2a7ffb39a1bcb3c3b76db45c0db3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11429654$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hammad, F T</creatorcontrib><creatorcontrib>Wheatley, A M</creatorcontrib><creatorcontrib>Davis, G</creatorcontrib><title>Role of endothelin ET(A) receptor antagonism in the post-transplant renal response to angiotensin II in the rat</title><title>Experimental physiology</title><addtitle>Exp Physiol</addtitle><description>The role of endothelins in the renal damage associated with ischaemic-reperfusion (I-R) injury during organ transplantation
was determined by selective blockade of the ET(A) receptors with the receptor antagonist ABT-627. The integrity of kidney
function was determined 2 and 8 weeks after transplantation by investigation of the renal response to angiotensin II. Under
pentobarbitone anaesthesia (70 mg x kg(-1), I.P.), rats underwent a right nephrectomy. Transplantation of the left kidney
was performed after 2 h cold ischaemia without or with ABT-627 treatment. Control animals underwent left renal denervation.
The renal response to angiotensin II was measured 2 weeks later following blockade of endogenous production of angiotensin
II with captopril. A further transplant group was allowed to recover for 8 weeks before the terminal study. In the control
group, angiotensin II reduced renal blood flow (RBF), glomerular filtration rate (GFR), urine flow rate (UV), and fractional
sodium excretion (FE(Na)) by 29 +/- 5 %, 19 +/- 4 %, 25 +/- 4 % and 32 +/- 7 %, respectively. Conversely, in the transplant
group, angiotensin II left RBF unchanged and increased GFR (59 +/- 12 %) and UV (93 +/- 8 %). FE(Na) decreased by 24 +/- 9
%. In both the transplant group treated with ABT-627 and the long-term recovery group, the renal response to angiotensin II
was normalised. In conclusion, renal transplantation following 2 h cold I-R injury resulted in a temporary abnormal renal
response to angiotensin II, which was reversed by ET(A) receptor antagonism at the time of transplantation.</description><subject>Angiotensin II - antagonists & inhibitors</subject><subject>Angiotensin II - metabolism</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Captopril - pharmacology</subject><subject>Cold Temperature</subject><subject>Endothelin Receptor Antagonists</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Glomerular Filtration Rate - physiology</subject><subject>Ischemia - physiopathology</subject><subject>Kidney Transplantation</subject><subject>Male</subject><subject>Pyrrolidines - pharmacology</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Receptor, Endothelin A</subject><subject>Renal Circulation - drug effects</subject><subject>Renal Circulation - physiology</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Renin-Angiotensin System - physiology</subject><subject>Sodium - urine</subject><issn>0958-0670</issn><issn>1469-445X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN1LwzAUxYMobn68-AdIn0SFatKkSfs4hh8DQRAF30KS3q6RrqlJhuy_N7LJXu59OL9z7uUgdEHwHSGE3sPYVRwXhIoDNCWM1zlj5echmuK6rHLMBZ6gkxC-MCYUV-wYTQhhRc1LNkXuzfWQuTaDoXGxg94O2cP79ewm82BgjM5naohq6QYbVlkSE5ONLsQ8ejWEsU9qQgfVpxlGNwTIokuepXURhpAci8W_z6t4ho5a1Qc43-1T9PH48D5_zl9enxbz2UtuCCcsN2UjTN3opiiKugFuQIEuuS5NIbAwuuaqVYUSbatprYg2mhqqBW80Kw1uND1FV9vc0bvvNYQoVzYY6NO_4NZBClxXTBCewNstaLwLwUMrR29Xym8kwfKvXrmvN8GXu9S1XkGzR3d97s92dtn9WA9y7DbBuuCMhbiRFZdUUl7SX55DhZM</recordid><startdate>20010501</startdate><enddate>20010501</enddate><creator>Hammad, F T</creator><creator>Wheatley, A M</creator><creator>Davis, G</creator><general>The Physiological Society</general><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>7X8</scope></search><sort><creationdate>20010501</creationdate><title>Role of endothelin ET(A) receptor antagonism in the post-transplant renal response to angiotensin II in the rat</title><author>Hammad, F T ; Wheatley, A M ; Davis, G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1614-c5d7c9dbd2229de6ceaeb56b5c2707cb96afa2a7ffb39a1bcb3c3b76db45c0db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Angiotensin II - antagonists & inhibitors</topic><topic>Angiotensin II - metabolism</topic><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Captopril - pharmacology</topic><topic>Cold Temperature</topic><topic>Endothelin Receptor Antagonists</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Glomerular Filtration Rate - physiology</topic><topic>Ischemia - physiopathology</topic><topic>Kidney Transplantation</topic><topic>Male</topic><topic>Pyrrolidines - pharmacology</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Receptor, Endothelin A</topic><topic>Renal Circulation - drug effects</topic><topic>Renal Circulation - physiology</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Renin-Angiotensin System - physiology</topic><topic>Sodium - urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hammad, F T</creatorcontrib><creatorcontrib>Wheatley, A M</creatorcontrib><creatorcontrib>Davis, G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hammad, F T</au><au>Wheatley, A M</au><au>Davis, G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of endothelin ET(A) receptor antagonism in the post-transplant renal response to angiotensin II in the rat</atitle><jtitle>Experimental physiology</jtitle><addtitle>Exp Physiol</addtitle><date>2001-05-01</date><risdate>2001</risdate><volume>86</volume><issue>3</issue><spage>365</spage><epage>372</epage><pages>365-372</pages><issn>0958-0670</issn><eissn>1469-445X</eissn><abstract>The role of endothelins in the renal damage associated with ischaemic-reperfusion (I-R) injury during organ transplantation
was determined by selective blockade of the ET(A) receptors with the receptor antagonist ABT-627. The integrity of kidney
function was determined 2 and 8 weeks after transplantation by investigation of the renal response to angiotensin II. Under
pentobarbitone anaesthesia (70 mg x kg(-1), I.P.), rats underwent a right nephrectomy. Transplantation of the left kidney
was performed after 2 h cold ischaemia without or with ABT-627 treatment. Control animals underwent left renal denervation.
The renal response to angiotensin II was measured 2 weeks later following blockade of endogenous production of angiotensin
II with captopril. A further transplant group was allowed to recover for 8 weeks before the terminal study. In the control
group, angiotensin II reduced renal blood flow (RBF), glomerular filtration rate (GFR), urine flow rate (UV), and fractional
sodium excretion (FE(Na)) by 29 +/- 5 %, 19 +/- 4 %, 25 +/- 4 % and 32 +/- 7 %, respectively. Conversely, in the transplant
group, angiotensin II left RBF unchanged and increased GFR (59 +/- 12 %) and UV (93 +/- 8 %). FE(Na) decreased by 24 +/- 9
%. In both the transplant group treated with ABT-627 and the long-term recovery group, the renal response to angiotensin II
was normalised. In conclusion, renal transplantation following 2 h cold I-R injury resulted in a temporary abnormal renal
response to angiotensin II, which was reversed by ET(A) receptor antagonism at the time of transplantation.</abstract><cop>England</cop><pub>The Physiological Society</pub><pmid>11429654</pmid><doi>10.1113/eph8602137</doi><tpages>8</tpages></addata></record> |
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| source | MEDLINE; Wiley Journals; Wiley Free Content |
| subjects | Angiotensin II - antagonists & inhibitors Angiotensin II - metabolism Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Blood Pressure - drug effects Blood Pressure - physiology Captopril - pharmacology Cold Temperature Endothelin Receptor Antagonists Glomerular Filtration Rate - drug effects Glomerular Filtration Rate - physiology Ischemia - physiopathology Kidney Transplantation Male Pyrrolidines - pharmacology Rats Rats, Inbred Lew Receptor, Endothelin A Renal Circulation - drug effects Renal Circulation - physiology Renin-Angiotensin System - drug effects Renin-Angiotensin System - physiology Sodium - urine |
| title | Role of endothelin ET(A) receptor antagonism in the post-transplant renal response to angiotensin II in the rat |
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