Effects of losartan and captopril on endothelin-1 production in blood vessels and glomeruli of rats with reduced renal mass
Recently, we have reported that endothelin-1 (ET-1) production is increased in blood vessels and glomeruli of rats with chronic renal failure. This study was design to investigate the role of angiotensin II (Ang II) in endogenous ET-1 production in rats with reduced renal mass. One week after subtot...
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| Veröffentlicht in: | American journal of hypertension 1998-08, Vol.11 (8), p.989-997 |
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| description | Recently, we have reported that endothelin-1 (ET-1) production is increased in blood vessels and glomeruli of rats with chronic renal failure. This study was design to investigate the role of angiotensin II (Ang II) in endogenous ET-1 production in rats with reduced renal mass. One week after subtotal (5/6) nephrectomy, uremic rats were divided into three groups, and received either no treatment, the Ang II subtype 1 receptor (AT1) antagonist losartan (10 mg/kg/day), or the angiotensin-converting enzyme inhibitor (ACE-I) captopril (30 mg/kg/day) for 6 weeks. Sham-operated rats were used as controls and received no treatment. The levels of immunoreactive ET-1 (ir-ET-1) in plasma and urine, as well as in vascular and renal tissues, were determined by radioimmunoassay (RIA) after extraction. In uremic rats, losartan and captopril completely prevented the increase in systolic blood pressure. At week 6, plasma ir-ET-1 was similar in the different groups of uremic rats and in the controls. However, ir-ET-1 concentration in the mesenteric arterial bed, the thoracic aorta, preglomerular arteries, and glomeruli, as well as urinary ir-ET-1 excretion were significantly greater in uremic-untreated rats compared to controls (P < .01). Treatment of uremic rats with losartan or captopril reduced ir-ET-1 concentration in the thoracic aorta and preglomerular arteries (P < .05), but ir-ET-1 concentration in the mesenteric arterial bed was unchanged. Although both drugs completely prevented the increase in proteinuria, losartan but not captopril significantly reduced ir-ET-1 concentration in glomeruli (P < .05) and normalized urinary ir-ET-1 excretion. This indicates that increased ET-1 production in blood vessels and glomeruli of uremic rats is modulated, at least in part, by Ang II through the AT1 receptor. The beneficial effects of the AT1 antagonist losartan could be attributable to the attenuation of Ang II-induced ET-1 production in this rat remnant kidney model of chronic renal failure, whereas those of the ACE-I captopril are not related to changes in ET-1 production in glomeruli. |
| doi_str_mv | 10.1016/S0895-7061(98)00088-0 |
| format | Article |
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This study was design to investigate the role of angiotensin II (Ang II) in endogenous ET-1 production in rats with reduced renal mass. One week after subtotal (5/6) nephrectomy, uremic rats were divided into three groups, and received either no treatment, the Ang II subtype 1 receptor (AT1) antagonist losartan (10 mg/kg/day), or the angiotensin-converting enzyme inhibitor (ACE-I) captopril (30 mg/kg/day) for 6 weeks. Sham-operated rats were used as controls and received no treatment. The levels of immunoreactive ET-1 (ir-ET-1) in plasma and urine, as well as in vascular and renal tissues, were determined by radioimmunoassay (RIA) after extraction. In uremic rats, losartan and captopril completely prevented the increase in systolic blood pressure. At week 6, plasma ir-ET-1 was similar in the different groups of uremic rats and in the controls. However, ir-ET-1 concentration in the mesenteric arterial bed, the thoracic aorta, preglomerular arteries, and glomeruli, as well as urinary ir-ET-1 excretion were significantly greater in uremic-untreated rats compared to controls (P < .01). Treatment of uremic rats with losartan or captopril reduced ir-ET-1 concentration in the thoracic aorta and preglomerular arteries (P < .05), but ir-ET-1 concentration in the mesenteric arterial bed was unchanged. Although both drugs completely prevented the increase in proteinuria, losartan but not captopril significantly reduced ir-ET-1 concentration in glomeruli (P < .05) and normalized urinary ir-ET-1 excretion. This indicates that increased ET-1 production in blood vessels and glomeruli of uremic rats is modulated, at least in part, by Ang II through the AT1 receptor. The beneficial effects of the AT1 antagonist losartan could be attributable to the attenuation of Ang II-induced ET-1 production in this rat remnant kidney model of chronic renal failure, whereas those of the ACE-I captopril are not related to changes in ET-1 production in glomeruli.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1879-1905</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/S0895-7061(98)00088-0</identifier><identifier>PMID: 9715793</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>angiotensin II ; Angiotensin II - physiology ; Animals ; Antihypertensive agents ; Biological and medical sciences ; Blood Pressure - drug effects ; blood vessels ; Blood Vessels - metabolism ; captopril ; Captopril - pharmacology ; Cardiovascular system ; chronic renal failure ; Endothelin-1 ; Endothelin-1 - biosynthesis ; glomeruli ; hypertension ; Kidney Failure, Chronic - metabolism ; Kidney Glomerulus - metabolism ; losartan ; Losartan - pharmacology ; Male ; Medical sciences ; Nephrectomy ; Pharmacology. Drug treatments ; Rats ; Rats, Sprague-Dawley</subject><ispartof>American journal of hypertension, 1998-08, Vol.11 (8), p.989-997</ispartof><rights>1998 American Journal of Hypertension, Ltd.</rights><rights>American Journal of Hypertension, Ltd. © 1998 by the American Journal of Hypertension, Ltd. 1998</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c515t-20388810ceae6b99614550ad8317763930c259ba2fa993d2ebad0f8126ebfcce3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2386760$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9715793$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Larivière, Richard</creatorcontrib><creatorcontrib>Lebel, Marcel</creatorcontrib><creatorcontrib>Kingma, Iris</creatorcontrib><creatorcontrib>Grose, JohnH</creatorcontrib><creatorcontrib>Boucher, Daniel</creatorcontrib><title>Effects of losartan and captopril on endothelin-1 production in blood vessels and glomeruli of rats with reduced renal mass</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>Recently, we have reported that endothelin-1 (ET-1) production is increased in blood vessels and glomeruli of rats with chronic renal failure. This study was design to investigate the role of angiotensin II (Ang II) in endogenous ET-1 production in rats with reduced renal mass. One week after subtotal (5/6) nephrectomy, uremic rats were divided into three groups, and received either no treatment, the Ang II subtype 1 receptor (AT1) antagonist losartan (10 mg/kg/day), or the angiotensin-converting enzyme inhibitor (ACE-I) captopril (30 mg/kg/day) for 6 weeks. Sham-operated rats were used as controls and received no treatment. The levels of immunoreactive ET-1 (ir-ET-1) in plasma and urine, as well as in vascular and renal tissues, were determined by radioimmunoassay (RIA) after extraction. In uremic rats, losartan and captopril completely prevented the increase in systolic blood pressure. At week 6, plasma ir-ET-1 was similar in the different groups of uremic rats and in the controls. However, ir-ET-1 concentration in the mesenteric arterial bed, the thoracic aorta, preglomerular arteries, and glomeruli, as well as urinary ir-ET-1 excretion were significantly greater in uremic-untreated rats compared to controls (P < .01). Treatment of uremic rats with losartan or captopril reduced ir-ET-1 concentration in the thoracic aorta and preglomerular arteries (P < .05), but ir-ET-1 concentration in the mesenteric arterial bed was unchanged. Although both drugs completely prevented the increase in proteinuria, losartan but not captopril significantly reduced ir-ET-1 concentration in glomeruli (P < .05) and normalized urinary ir-ET-1 excretion. This indicates that increased ET-1 production in blood vessels and glomeruli of uremic rats is modulated, at least in part, by Ang II through the AT1 receptor. The beneficial effects of the AT1 antagonist losartan could be attributable to the attenuation of Ang II-induced ET-1 production in this rat remnant kidney model of chronic renal failure, whereas those of the ACE-I captopril are not related to changes in ET-1 production in glomeruli.</description><subject>angiotensin II</subject><subject>Angiotensin II - physiology</subject><subject>Animals</subject><subject>Antihypertensive agents</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>blood vessels</subject><subject>Blood Vessels - metabolism</subject><subject>captopril</subject><subject>Captopril - pharmacology</subject><subject>Cardiovascular system</subject><subject>chronic renal failure</subject><subject>Endothelin-1</subject><subject>Endothelin-1 - biosynthesis</subject><subject>glomeruli</subject><subject>hypertension</subject><subject>Kidney Failure, Chronic - metabolism</subject><subject>Kidney Glomerulus - metabolism</subject><subject>losartan</subject><subject>Losartan - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrectomy</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>0895-7061</issn><issn>1879-1905</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk-LFDEQxRtR1nH1IyzkIKKHaNLZ_DuJDKsrLoiMgngJ6XS1G80ks0n3qvjlTU8PA4LgqSD1e6-SV2maM0qeU0LFiw1RmmNJBH2q1TNCiFKY3GlWVEmNqSb8brM6IvebB6V8q9C5EPSkOdGScqnZqvl9MQzgxoLSgEIqNo82Iht75OxuTLvsA0oRQezTeA3BR0zRLqd-cqOv5z6iLqTUo1soBULZK7-GtIU8BT97Zlu9f_jxGmWoKuhrjTagrS3lYXNvsKHAo0M9bT69vvi4vsRX79-8Xb-6wo5TPuKWMKUUJQ4siE5rQc85J7ZXjEopmGbEtVx3th2s1qxvobM9GRRtBXSDc8BOmyeLb735zQRlNFtfHIRgI6SpGMkUZ1TzCvIFdDmVkmEwNYCtzb8MJWYO3exDN3OiRiuzD92Qqjs7DJi6LfRH1SHl2n986NvibBiyjc6XI9YyJaSYbciCpWn378n4r8l4luBF4ssIP48im78bIZnk5vLzF7N-90FvdLsxtPIvF74uC249ZFOch1j34nP9BqZP_j9v_QO5ebxy</recordid><startdate>19980801</startdate><enddate>19980801</enddate><creator>Larivière, Richard</creator><creator>Lebel, Marcel</creator><creator>Kingma, Iris</creator><creator>Grose, JohnH</creator><creator>Boucher, Daniel</creator><general>Elsevier Inc</general><general>Oxford University Press</general><general>Elsevier Science</general><scope>BSCLL</scope><scope>IQODW</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>7X8</scope></search><sort><creationdate>19980801</creationdate><title>Effects of losartan and captopril on endothelin-1 production in blood vessels and glomeruli of rats with reduced renal mass</title><author>Larivière, Richard ; Lebel, Marcel ; Kingma, Iris ; Grose, JohnH ; Boucher, Daniel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c515t-20388810ceae6b99614550ad8317763930c259ba2fa993d2ebad0f8126ebfcce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>angiotensin II</topic><topic>Angiotensin II - physiology</topic><topic>Animals</topic><topic>Antihypertensive agents</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>blood vessels</topic><topic>Blood Vessels - metabolism</topic><topic>captopril</topic><topic>Captopril - pharmacology</topic><topic>Cardiovascular system</topic><topic>chronic renal failure</topic><topic>Endothelin-1</topic><topic>Endothelin-1 - biosynthesis</topic><topic>glomeruli</topic><topic>hypertension</topic><topic>Kidney Failure, Chronic - metabolism</topic><topic>Kidney Glomerulus - metabolism</topic><topic>losartan</topic><topic>Losartan - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrectomy</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Larivière, Richard</creatorcontrib><creatorcontrib>Lebel, Marcel</creatorcontrib><creatorcontrib>Kingma, Iris</creatorcontrib><creatorcontrib>Grose, JohnH</creatorcontrib><creatorcontrib>Boucher, Daniel</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><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>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Larivière, Richard</au><au>Lebel, Marcel</au><au>Kingma, Iris</au><au>Grose, JohnH</au><au>Boucher, Daniel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of losartan and captopril on endothelin-1 production in blood vessels and glomeruli of rats with reduced renal mass</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>1998-08-01</date><risdate>1998</risdate><volume>11</volume><issue>8</issue><spage>989</spage><epage>997</epage><pages>989-997</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><abstract>Recently, we have reported that endothelin-1 (ET-1) production is increased in blood vessels and glomeruli of rats with chronic renal failure. This study was design to investigate the role of angiotensin II (Ang II) in endogenous ET-1 production in rats with reduced renal mass. One week after subtotal (5/6) nephrectomy, uremic rats were divided into three groups, and received either no treatment, the Ang II subtype 1 receptor (AT1) antagonist losartan (10 mg/kg/day), or the angiotensin-converting enzyme inhibitor (ACE-I) captopril (30 mg/kg/day) for 6 weeks. Sham-operated rats were used as controls and received no treatment. The levels of immunoreactive ET-1 (ir-ET-1) in plasma and urine, as well as in vascular and renal tissues, were determined by radioimmunoassay (RIA) after extraction. In uremic rats, losartan and captopril completely prevented the increase in systolic blood pressure. At week 6, plasma ir-ET-1 was similar in the different groups of uremic rats and in the controls. However, ir-ET-1 concentration in the mesenteric arterial bed, the thoracic aorta, preglomerular arteries, and glomeruli, as well as urinary ir-ET-1 excretion were significantly greater in uremic-untreated rats compared to controls (P < .01). Treatment of uremic rats with losartan or captopril reduced ir-ET-1 concentration in the thoracic aorta and preglomerular arteries (P < .05), but ir-ET-1 concentration in the mesenteric arterial bed was unchanged. Although both drugs completely prevented the increase in proteinuria, losartan but not captopril significantly reduced ir-ET-1 concentration in glomeruli (P < .05) and normalized urinary ir-ET-1 excretion. This indicates that increased ET-1 production in blood vessels and glomeruli of uremic rats is modulated, at least in part, by Ang II through the AT1 receptor. The beneficial effects of the AT1 antagonist losartan could be attributable to the attenuation of Ang II-induced ET-1 production in this rat remnant kidney model of chronic renal failure, whereas those of the ACE-I captopril are not related to changes in ET-1 production in glomeruli.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>9715793</pmid><doi>10.1016/S0895-7061(98)00088-0</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | American journal of hypertension, 1998-08, Vol.11 (8), p.989-997 |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Alma/SFX Local Collection |
| subjects | angiotensin II Angiotensin II - physiology Animals Antihypertensive agents Biological and medical sciences Blood Pressure - drug effects blood vessels Blood Vessels - metabolism captopril Captopril - pharmacology Cardiovascular system chronic renal failure Endothelin-1 Endothelin-1 - biosynthesis glomeruli hypertension Kidney Failure, Chronic - metabolism Kidney Glomerulus - metabolism losartan Losartan - pharmacology Male Medical sciences Nephrectomy Pharmacology. Drug treatments Rats Rats, Sprague-Dawley |
| title | Effects of losartan and captopril on endothelin-1 production in blood vessels and glomeruli of rats with reduced renal mass |
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