ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus
ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus. The enormous contribution of renin-angiotensin system (RAS) interruption with ACE (angiotensin-converting enzyme) inhibitors and angiotensin II receptor blockers (ARB) in the treatment of diabeti...
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| Veröffentlicht in: | Kidney international 2005-03, Vol.67 (3), p.1033-1037 |
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| creator | Cecilia Lansang, M. Stevanovic, Radomir Price, Deborah A. Laffel, Lori M.B. Hollenberg, Norman K. |
| description | ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus.
The enormous contribution of renin-angiotensin system (RAS) interruption with ACE (angiotensin-converting enzyme) inhibitors and angiotensin II receptor blockers (ARB) in the treatment of diabetic nephropathy has led to interest in the factors involved in angiotensin II (Ang II) generation. In normal subjects, RAS interruption using an ARB produced a 50% greater renal plasma flow (RPF) rise than with an ACE inhibitor, suggesting a substantial contribution of non-ACE pathways. Moreover, immunohistochemistry studies in kidneys of overtly proteinuric diabetic subjects showed up-regulation of chymase, an alternative Ang II-generating enzyme. Our aim was to determine the degree to which the non-ACE pathways contribute to RAS activation in type 1 diabetes mellitus (DM).
Type 1DM patients (N = 37, 14 M/23 F; age 31 ± 2 years; DM duration 16 ± 1.7 years; HbA1c 7.7.0 ± 0.3%) were studied on a high-salt diet. They received captopril 25mg po one day and candesartan 16mg po the next day. RPF and glomerular filtration rate (GFR) were measured before and up to 4 hours after drug administration.
Both captopril and candesartan induced a significant rise in RPF (baseline vs. peak |
| doi_str_mv | 10.1111/j.1523-1755.2005.00167.x |
| format | Article |
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The enormous contribution of renin-angiotensin system (RAS) interruption with ACE (angiotensin-converting enzyme) inhibitors and angiotensin II receptor blockers (ARB) in the treatment of diabetic nephropathy has led to interest in the factors involved in angiotensin II (Ang II) generation. In normal subjects, RAS interruption using an ARB produced a 50% greater renal plasma flow (RPF) rise than with an ACE inhibitor, suggesting a substantial contribution of non-ACE pathways. Moreover, immunohistochemistry studies in kidneys of overtly proteinuric diabetic subjects showed up-regulation of chymase, an alternative Ang II-generating enzyme. Our aim was to determine the degree to which the non-ACE pathways contribute to RAS activation in type 1 diabetes mellitus (DM).
Type 1DM patients (N = 37, 14 M/23 F; age 31 ± 2 years; DM duration 16 ± 1.7 years; HbA1c 7.7.0 ± 0.3%) were studied on a high-salt diet. They received captopril 25mg po one day and candesartan 16mg po the next day. RPF and glomerular filtration rate (GFR) were measured before and up to 4 hours after drug administration.
Both captopril and candesartan induced a significant rise in RPF (baseline vs. peak <0.0001 for both), and the rise was concordant for the 2 drugs (r = 0.77,P < 0.001). However, the RPF responses were not significantly different between the 2 drugs (captopril 72 ± 11mL/min/1.73m2, candesartan 75 ± 12,P = 0.841).
In predominantly normoalbuminuric, normotensive type 1 DM, activation of the intrarenal RAS reflects a mechanism involving primarily the classic ACE pathway.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1111/j.1523-1755.2005.00167.x</identifier><identifier>PMID: 15698442</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Benzimidazoles - pharmacology ; Biological and medical sciences ; Captopril - pharmacology ; chymase ; diabetes mellitus ; Diabetes Mellitus, Type 1 - physiopathology ; Female ; Glomerular Filtration Rate - drug effects ; Humans ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Peptidyl-Dipeptidase A - physiology ; Renal Circulation - drug effects ; renal hemodynamics ; renin-angiotensin system ; Renin-Angiotensin System - physiology ; Tetrazoles - pharmacology</subject><ispartof>Kidney international, 2005-03, Vol.67 (3), p.1033-1037</ispartof><rights>2005 International Society of Nephrology</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533t-36c77ebe8b2f103f389c1db63b1ef2d9560bedeefad516e194674994ec3bf7893</citedby><cites>FETCH-LOGICAL-c533t-36c77ebe8b2f103f389c1db63b1ef2d9560bedeefad516e194674994ec3bf7893</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210120703?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16589685$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15698442$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cecilia Lansang, M.</creatorcontrib><creatorcontrib>Stevanovic, Radomir</creatorcontrib><creatorcontrib>Price, Deborah A.</creatorcontrib><creatorcontrib>Laffel, Lori M.B.</creatorcontrib><creatorcontrib>Hollenberg, Norman K.</creatorcontrib><title>ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus.
The enormous contribution of renin-angiotensin system (RAS) interruption with ACE (angiotensin-converting enzyme) inhibitors and angiotensin II receptor blockers (ARB) in the treatment of diabetic nephropathy has led to interest in the factors involved in angiotensin II (Ang II) generation. In normal subjects, RAS interruption using an ARB produced a 50% greater renal plasma flow (RPF) rise than with an ACE inhibitor, suggesting a substantial contribution of non-ACE pathways. Moreover, immunohistochemistry studies in kidneys of overtly proteinuric diabetic subjects showed up-regulation of chymase, an alternative Ang II-generating enzyme. Our aim was to determine the degree to which the non-ACE pathways contribute to RAS activation in type 1 diabetes mellitus (DM).
Type 1DM patients (N = 37, 14 M/23 F; age 31 ± 2 years; DM duration 16 ± 1.7 years; HbA1c 7.7.0 ± 0.3%) were studied on a high-salt diet. They received captopril 25mg po one day and candesartan 16mg po the next day. RPF and glomerular filtration rate (GFR) were measured before and up to 4 hours after drug administration.
Both captopril and candesartan induced a significant rise in RPF (baseline vs. peak <0.0001 for both), and the rise was concordant for the 2 drugs (r = 0.77,P < 0.001). However, the RPF responses were not significantly different between the 2 drugs (captopril 72 ± 11mL/min/1.73m2, candesartan 75 ± 12,P = 0.841).
In predominantly normoalbuminuric, normotensive type 1 DM, activation of the intrarenal RAS reflects a mechanism involving primarily the classic ACE pathway.</description><subject>Adult</subject><subject>Benzimidazoles - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Captopril - pharmacology</subject><subject>chymase</subject><subject>diabetes mellitus</subject><subject>Diabetes Mellitus, Type 1 - physiopathology</subject><subject>Female</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Peptidyl-Dipeptidase A - physiology</subject><subject>Renal Circulation - drug effects</subject><subject>renal hemodynamics</subject><subject>renin-angiotensin system</subject><subject>Renin-Angiotensin System - physiology</subject><subject>Tetrazoles - pharmacology</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU1v1DAQQC0EokvhJ4AsJOCUYMexYx-3q0KRKlXi42w5zoR6lXWC7ZTuv8fprlqpB-qLPZo3oxk_hDAlJc3n87akvGIFbTgvK0J4SQgVTXn7DK3uE8_RihDJi4ozeYJexbglOVaMvEQnlAsl67paod_rzTk2vsN-9MXynky6_mv2ETuP0zXgAN4M-MZEOw8m5DBOo4-A04i_r39kKkEI85Tc6O9K9hNgijtnWkgQ8Q6GwaU5vkYvejNEeHO8T9GvL-c_NxfF5dXXb5v1ZWE5Y6lgwjYNtCDbqqeE9UwqS7tWsJZCX3WKC9JCB9CbjlMBVNWiqZWqwbK2b_J2p-jToe8Uxj8zxKR3Lto8hPEwzlFLprgUkotMfvwvmRvTphEL-P4RuB3nkH8l6ooSWpGGsAzJA2TDGGOAXk_B7UzYa0r04kxv9aJGL2r04kzfOdO3ufTdsf_c7qB7KDxKysCHI5AtmKEPxlsXHzjBpcorZe7tgfMmzQHugbpWnLJlkbNDHrKAGwdBR-vAW-hcAJt0N7qnp_0H-3W97Q</recordid><startdate>20050301</startdate><enddate>20050301</enddate><creator>Cecilia Lansang, M.</creator><creator>Stevanovic, Radomir</creator><creator>Price, Deborah A.</creator><creator>Laffel, Lori M.B.</creator><creator>Hollenberg, Norman K.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>20050301</creationdate><title>ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus</title><author>Cecilia Lansang, M. ; Stevanovic, Radomir ; Price, Deborah A. ; Laffel, Lori M.B. ; Hollenberg, Norman K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c533t-36c77ebe8b2f103f389c1db63b1ef2d9560bedeefad516e194674994ec3bf7893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Benzimidazoles - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Captopril - pharmacology</topic><topic>chymase</topic><topic>diabetes mellitus</topic><topic>Diabetes Mellitus, Type 1 - physiopathology</topic><topic>Female</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Peptidyl-Dipeptidase A - physiology</topic><topic>Renal Circulation - drug effects</topic><topic>renal hemodynamics</topic><topic>renin-angiotensin system</topic><topic>Renin-Angiotensin System - physiology</topic><topic>Tetrazoles - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cecilia Lansang, M.</creatorcontrib><creatorcontrib>Stevanovic, Radomir</creatorcontrib><creatorcontrib>Price, Deborah A.</creatorcontrib><creatorcontrib>Laffel, Lori M.B.</creatorcontrib><creatorcontrib>Hollenberg, Norman K.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cecilia Lansang, M.</au><au>Stevanovic, Radomir</au><au>Price, Deborah A.</au><au>Laffel, Lori M.B.</au><au>Hollenberg, Norman K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2005-03-01</date><risdate>2005</risdate><volume>67</volume><issue>3</issue><spage>1033</spage><epage>1037</epage><pages>1033-1037</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus.
The enormous contribution of renin-angiotensin system (RAS) interruption with ACE (angiotensin-converting enzyme) inhibitors and angiotensin II receptor blockers (ARB) in the treatment of diabetic nephropathy has led to interest in the factors involved in angiotensin II (Ang II) generation. In normal subjects, RAS interruption using an ARB produced a 50% greater renal plasma flow (RPF) rise than with an ACE inhibitor, suggesting a substantial contribution of non-ACE pathways. Moreover, immunohistochemistry studies in kidneys of overtly proteinuric diabetic subjects showed up-regulation of chymase, an alternative Ang II-generating enzyme. Our aim was to determine the degree to which the non-ACE pathways contribute to RAS activation in type 1 diabetes mellitus (DM).
Type 1DM patients (N = 37, 14 M/23 F; age 31 ± 2 years; DM duration 16 ± 1.7 years; HbA1c 7.7.0 ± 0.3%) were studied on a high-salt diet. They received captopril 25mg po one day and candesartan 16mg po the next day. RPF and glomerular filtration rate (GFR) were measured before and up to 4 hours after drug administration.
Both captopril and candesartan induced a significant rise in RPF (baseline vs. peak <0.0001 for both), and the rise was concordant for the 2 drugs (r = 0.77,P < 0.001). However, the RPF responses were not significantly different between the 2 drugs (captopril 72 ± 11mL/min/1.73m2, candesartan 75 ± 12,P = 0.841).
In predominantly normoalbuminuric, normotensive type 1 DM, activation of the intrarenal RAS reflects a mechanism involving primarily the classic ACE pathway.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15698442</pmid><doi>10.1111/j.1523-1755.2005.00167.x</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Benzimidazoles - pharmacology Biological and medical sciences Captopril - pharmacology chymase diabetes mellitus Diabetes Mellitus, Type 1 - physiopathology Female Glomerular Filtration Rate - drug effects Humans Male Medical sciences Nephrology. Urinary tract diseases Peptidyl-Dipeptidase A - physiology Renal Circulation - drug effects renal hemodynamics renin-angiotensin system Renin-Angiotensin System - physiology Tetrazoles - pharmacology |
| title | ACE and non-ACE pathways in the renal vascular response to RAS interruption in type 1 diabetes mellitus |
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