Sequential activation of the intrarenal renin-angiotensin system in the progression of hypertensive nephropathy in Goldblatt rats
The intrarenal renin-angiotensin system (RAS) has an important role in generating and maintaining hypertension in two-kidney, one-clip (2K1C) rats. This study evaluated how various intrarenal RAS components contributed to hypertension not only in the maintenance period (5w; 5 wk after operation) but...
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container_title | American journal of physiology. Renal physiology |
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creator | Kim, Yang Gyun Lee, Sang Ho Kim, Se-Yun Lee, Arah Moon, Ju Young Jeong, Kyung-Hwan Lee, Tae Won Lim, Sung Jig Sohn, Il Suk Ihm, Chun-Gyoo |
description | The intrarenal renin-angiotensin system (RAS) has an important role in generating and maintaining hypertension in two-kidney, one-clip (2K1C) rats. This study evaluated how various intrarenal RAS components contributed to hypertension not only in the maintenance period (5w; 5 wk after operation) but also earlier (2w; 2 wk after operation). We inserted a 2.5-mm clip into the left renal artery of Sprague-Dawley rats and euthanized them at 2w and 5w following the operation. Systolic blood pressure increased within 1 wk after the operation, and left ventricular hypertrophy occurred in 2K1C rats. At 2w, juxtaglomerular apparatus (JGA) and collecting duct (CD) renin increased in clipped kidney (CK) of 2K1C rats. The tubular angiotensin I-converting enzyme (ACE) was not changed, but peritubular ACE2 decreased in nonclipped kidney (NCK) and CK of 2K1C rats. At 5w, ACE and CD renin were enhanced, and ACE2 was still lessened in both kidneys of 2K1C rats. However, plasma renin activity (PRA) was not different from that in sham rats. In proximal tubules of CK, the ANG II type 1 receptor (AT1R) was not suppressed, but the Mas receptor (MasR) was reduced; thus the AT1R/MasR ratio was elevated. Although hypoxic change in CK could not be excluded, the JGA renin of CK and CD renin in both kidneys was highly expressed independent of time. Peritubular ACE2 changed in the earlier period, and uninhibited AT1R in proximal tubules of CK was presented in the maintenance period. In 2K1C rats, attenuated ACE2 seems to contribute to initiating hypertension while upregulated ACE in combination with unsuppressed AT1R may have a key role in maintaining hypertension. |
doi_str_mv | 10.1152/ajprenal.00001.2015 |
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This study evaluated how various intrarenal RAS components contributed to hypertension not only in the maintenance period (5w; 5 wk after operation) but also earlier (2w; 2 wk after operation). We inserted a 2.5-mm clip into the left renal artery of Sprague-Dawley rats and euthanized them at 2w and 5w following the operation. Systolic blood pressure increased within 1 wk after the operation, and left ventricular hypertrophy occurred in 2K1C rats. At 2w, juxtaglomerular apparatus (JGA) and collecting duct (CD) renin increased in clipped kidney (CK) of 2K1C rats. The tubular angiotensin I-converting enzyme (ACE) was not changed, but peritubular ACE2 decreased in nonclipped kidney (NCK) and CK of 2K1C rats. At 5w, ACE and CD renin were enhanced, and ACE2 was still lessened in both kidneys of 2K1C rats. However, plasma renin activity (PRA) was not different from that in sham rats. In proximal tubules of CK, the ANG II type 1 receptor (AT1R) was not suppressed, but the Mas receptor (MasR) was reduced; thus the AT1R/MasR ratio was elevated. Although hypoxic change in CK could not be excluded, the JGA renin of CK and CD renin in both kidneys was highly expressed independent of time. Peritubular ACE2 changed in the earlier period, and uninhibited AT1R in proximal tubules of CK was presented in the maintenance period. In 2K1C rats, attenuated ACE2 seems to contribute to initiating hypertension while upregulated ACE in combination with unsuppressed AT1R may have a key role in maintaining hypertension.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00001.2015</identifier><identifier>PMID: 26823279</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Blood Pressure ; Disease Progression ; Echocardiography ; Hypertension ; Hypertension, Renal - etiology ; Hypertension, Renal - physiopathology ; Hypertension, Renovascular - complications ; Hypertension, Renovascular - physiopathology ; Hypertrophy, Left Ventricular - diagnostic imaging ; Hypertrophy, Left Ventricular - etiology ; Hypoxia ; Juxtaglomerular Apparatus - pathology ; Kidney - physiopathology ; Kidney Tubules, Collecting - pathology ; Male ; Nephritis - etiology ; Nephritis - physiopathology ; Proteins ; Rats ; Rats, Sprague-Dawley ; Renin-Angiotensin System ; Rodents</subject><ispartof>American journal of physiology. Renal physiology, 2016-07, Vol.311 (1), p.F195-F206</ispartof><rights>Copyright © 2016 the American Physiological Society.</rights><rights>Copyright American Physiological Society Jul 1, 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c378t-99e3705f0ae8c5dbd49bd8a61775218265a27fbc660ea0cb51b036fa96a5bbc63</citedby><cites>FETCH-LOGICAL-c378t-99e3705f0ae8c5dbd49bd8a61775218265a27fbc660ea0cb51b036fa96a5bbc63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26823279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Yang Gyun</creatorcontrib><creatorcontrib>Lee, Sang Ho</creatorcontrib><creatorcontrib>Kim, Se-Yun</creatorcontrib><creatorcontrib>Lee, Arah</creatorcontrib><creatorcontrib>Moon, Ju Young</creatorcontrib><creatorcontrib>Jeong, Kyung-Hwan</creatorcontrib><creatorcontrib>Lee, Tae Won</creatorcontrib><creatorcontrib>Lim, Sung Jig</creatorcontrib><creatorcontrib>Sohn, Il Suk</creatorcontrib><creatorcontrib>Ihm, Chun-Gyoo</creatorcontrib><title>Sequential activation of the intrarenal renin-angiotensin system in the progression of hypertensive nephropathy in Goldblatt rats</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>The intrarenal renin-angiotensin system (RAS) has an important role in generating and maintaining hypertension in two-kidney, one-clip (2K1C) rats. This study evaluated how various intrarenal RAS components contributed to hypertension not only in the maintenance period (5w; 5 wk after operation) but also earlier (2w; 2 wk after operation). We inserted a 2.5-mm clip into the left renal artery of Sprague-Dawley rats and euthanized them at 2w and 5w following the operation. Systolic blood pressure increased within 1 wk after the operation, and left ventricular hypertrophy occurred in 2K1C rats. At 2w, juxtaglomerular apparatus (JGA) and collecting duct (CD) renin increased in clipped kidney (CK) of 2K1C rats. The tubular angiotensin I-converting enzyme (ACE) was not changed, but peritubular ACE2 decreased in nonclipped kidney (NCK) and CK of 2K1C rats. At 5w, ACE and CD renin were enhanced, and ACE2 was still lessened in both kidneys of 2K1C rats. However, plasma renin activity (PRA) was not different from that in sham rats. In proximal tubules of CK, the ANG II type 1 receptor (AT1R) was not suppressed, but the Mas receptor (MasR) was reduced; thus the AT1R/MasR ratio was elevated. Although hypoxic change in CK could not be excluded, the JGA renin of CK and CD renin in both kidneys was highly expressed independent of time. Peritubular ACE2 changed in the earlier period, and uninhibited AT1R in proximal tubules of CK was presented in the maintenance period. In 2K1C rats, attenuated ACE2 seems to contribute to initiating hypertension while upregulated ACE in combination with unsuppressed AT1R may have a key role in maintaining hypertension.</description><subject>Animals</subject><subject>Blood Pressure</subject><subject>Disease Progression</subject><subject>Echocardiography</subject><subject>Hypertension</subject><subject>Hypertension, Renal - etiology</subject><subject>Hypertension, Renal - physiopathology</subject><subject>Hypertension, Renovascular - complications</subject><subject>Hypertension, Renovascular - physiopathology</subject><subject>Hypertrophy, Left Ventricular - diagnostic imaging</subject><subject>Hypertrophy, Left Ventricular - etiology</subject><subject>Hypoxia</subject><subject>Juxtaglomerular Apparatus - pathology</subject><subject>Kidney - physiopathology</subject><subject>Kidney Tubules, Collecting - pathology</subject><subject>Male</subject><subject>Nephritis - etiology</subject><subject>Nephritis - physiopathology</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renin-Angiotensin System</subject><subject>Rodents</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUtLxDAUhYMoPkZ_gSAFN2465jFJ26WILxBcqOCu3La3Mxk6SU0yA7P0n5vW0YVZJOHmOyc3OYScMzplTPJrWPYODXRTGgebcsrkHjmOJzxlM6X2474QLM1l9nFETrxfDhjj7JAccZVzwbPimHy94ucaTdDQJVAHvYGgrUlsm4QFJtoEB-MlSZy1ScHMtQ1ovDaJ3_qAq8iMaO_s3KH3O_Vi26MbwQ0mBvuFsz2ExXbAH2zXVB2EkDgI_pQctNB5PNutE_J-f_d2-5g-vzw83d48p7XI8pAWBYqMypYC5rVsqmZWVE0OimWZ5CznSgLP2qpWiiLQupKsokK1UCiQVSyLCbn68Y2dxif7UK60r7HrwKBd-5LllM2EEFJE9PIfurRrF39hpPhMZjkdDMUPVTvrvcO27J1egduWjJZDQuVvQuWYUDkkFFUXO-91tcLmT_MbifgGR0GRqQ</recordid><startdate>20160701</startdate><enddate>20160701</enddate><creator>Kim, Yang Gyun</creator><creator>Lee, Sang Ho</creator><creator>Kim, Se-Yun</creator><creator>Lee, Arah</creator><creator>Moon, Ju Young</creator><creator>Jeong, Kyung-Hwan</creator><creator>Lee, Tae Won</creator><creator>Lim, Sung Jig</creator><creator>Sohn, Il Suk</creator><creator>Ihm, Chun-Gyoo</creator><general>American 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>20160701</creationdate><title>Sequential activation of the intrarenal renin-angiotensin system in the progression of hypertensive nephropathy in Goldblatt rats</title><author>Kim, Yang Gyun ; Lee, Sang Ho ; Kim, Se-Yun ; Lee, Arah ; Moon, Ju Young ; Jeong, Kyung-Hwan ; Lee, Tae Won ; Lim, Sung Jig ; Sohn, Il Suk ; Ihm, Chun-Gyoo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c378t-99e3705f0ae8c5dbd49bd8a61775218265a27fbc660ea0cb51b036fa96a5bbc63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Blood Pressure</topic><topic>Disease Progression</topic><topic>Echocardiography</topic><topic>Hypertension</topic><topic>Hypertension, Renal - etiology</topic><topic>Hypertension, Renal - physiopathology</topic><topic>Hypertension, Renovascular - complications</topic><topic>Hypertension, Renovascular - physiopathology</topic><topic>Hypertrophy, Left Ventricular - diagnostic imaging</topic><topic>Hypertrophy, Left Ventricular - etiology</topic><topic>Hypoxia</topic><topic>Juxtaglomerular Apparatus - pathology</topic><topic>Kidney - physiopathology</topic><topic>Kidney Tubules, Collecting - pathology</topic><topic>Male</topic><topic>Nephritis - etiology</topic><topic>Nephritis - physiopathology</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renin-Angiotensin System</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Yang Gyun</creatorcontrib><creatorcontrib>Lee, Sang Ho</creatorcontrib><creatorcontrib>Kim, Se-Yun</creatorcontrib><creatorcontrib>Lee, Arah</creatorcontrib><creatorcontrib>Moon, Ju Young</creatorcontrib><creatorcontrib>Jeong, Kyung-Hwan</creatorcontrib><creatorcontrib>Lee, Tae Won</creatorcontrib><creatorcontrib>Lim, Sung Jig</creatorcontrib><creatorcontrib>Sohn, Il Suk</creatorcontrib><creatorcontrib>Ihm, Chun-Gyoo</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>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Yang Gyun</au><au>Lee, Sang Ho</au><au>Kim, Se-Yun</au><au>Lee, Arah</au><au>Moon, Ju Young</au><au>Jeong, Kyung-Hwan</au><au>Lee, Tae Won</au><au>Lim, Sung Jig</au><au>Sohn, Il Suk</au><au>Ihm, Chun-Gyoo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sequential activation of the intrarenal renin-angiotensin system in the progression of hypertensive nephropathy in Goldblatt rats</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2016-07-01</date><risdate>2016</risdate><volume>311</volume><issue>1</issue><spage>F195</spage><epage>F206</epage><pages>F195-F206</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>The intrarenal renin-angiotensin system (RAS) has an important role in generating and maintaining hypertension in two-kidney, one-clip (2K1C) rats. This study evaluated how various intrarenal RAS components contributed to hypertension not only in the maintenance period (5w; 5 wk after operation) but also earlier (2w; 2 wk after operation). We inserted a 2.5-mm clip into the left renal artery of Sprague-Dawley rats and euthanized them at 2w and 5w following the operation. Systolic blood pressure increased within 1 wk after the operation, and left ventricular hypertrophy occurred in 2K1C rats. At 2w, juxtaglomerular apparatus (JGA) and collecting duct (CD) renin increased in clipped kidney (CK) of 2K1C rats. The tubular angiotensin I-converting enzyme (ACE) was not changed, but peritubular ACE2 decreased in nonclipped kidney (NCK) and CK of 2K1C rats. At 5w, ACE and CD renin were enhanced, and ACE2 was still lessened in both kidneys of 2K1C rats. However, plasma renin activity (PRA) was not different from that in sham rats. In proximal tubules of CK, the ANG II type 1 receptor (AT1R) was not suppressed, but the Mas receptor (MasR) was reduced; thus the AT1R/MasR ratio was elevated. Although hypoxic change in CK could not be excluded, the JGA renin of CK and CD renin in both kidneys was highly expressed independent of time. Peritubular ACE2 changed in the earlier period, and uninhibited AT1R in proximal tubules of CK was presented in the maintenance period. In 2K1C rats, attenuated ACE2 seems to contribute to initiating hypertension while upregulated ACE in combination with unsuppressed AT1R may have a key role in maintaining hypertension.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>26823279</pmid><doi>10.1152/ajprenal.00001.2015</doi><oa>free_for_read</oa></addata></record> |
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subjects | Animals Blood Pressure Disease Progression Echocardiography Hypertension Hypertension, Renal - etiology Hypertension, Renal - physiopathology Hypertension, Renovascular - complications Hypertension, Renovascular - physiopathology Hypertrophy, Left Ventricular - diagnostic imaging Hypertrophy, Left Ventricular - etiology Hypoxia Juxtaglomerular Apparatus - pathology Kidney - physiopathology Kidney Tubules, Collecting - pathology Male Nephritis - etiology Nephritis - physiopathology Proteins Rats Rats, Sprague-Dawley Renin-Angiotensin System Rodents |
title | Sequential activation of the intrarenal renin-angiotensin system in the progression of hypertensive nephropathy in Goldblatt rats |
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