Effect of aldosterone on renal transforming growth factor-beta
Aldosterone participates in the pathophysiology of several models of progressive chronic renal disease. Because of the causal connection between transforming growth factor-beta(1) (TGF-beta) and scarring in many such models, we hypothesized that aldosterone could evoke TGF-beta in the kidney. Aldost...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 2004-06, Vol.286 (6), p.F1059-F1062 |
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| container_issue | 6 |
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| container_title | American journal of physiology. Renal physiology |
| container_volume | 286 |
| creator | Juknevicius, Irmantas Segal, Yoav Kren, Stefan Lee, Rutha Hostetter, Thomas H |
| description | Aldosterone participates in the pathophysiology of several models of progressive chronic renal disease. Because of the causal connection between transforming growth factor-beta(1) (TGF-beta) and scarring in many such models, we hypothesized that aldosterone could evoke TGF-beta in the kidney. Aldosterone infusion for 3 days in otherwise normal rats caused a more than twofold increase in TGF-beta excretion without changes in systolic pressure or evidence of kidney damage. Concurrent treatment with amiloride did not alter this effect, indicating that aldosterone's stimulation of TGF-beta was independent of its regulation of sodium or potassium transport. However, concurrent treatment with spironolactone did block the increase in TGF-beta, indicating that the effect depends on the mineralocorticoid receptor. Renal mRNA for serum glucocorticoid kinase rose, but no change in TGF-beta message occurred, suggesting posttranscriptional enhancement of renal TGF-beta. In summary, aldosterone provokes renal TGF-beta, and this action may contribute to aldosterone's fibrotic propensity. |
| doi_str_mv | 10.1152/ajprenal.00202.2003 |
| format | Article |
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Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>Aldosterone participates in the pathophysiology of several models of progressive chronic renal disease. Because of the causal connection between transforming growth factor-beta(1) (TGF-beta) and scarring in many such models, we hypothesized that aldosterone could evoke TGF-beta in the kidney. Aldosterone infusion for 3 days in otherwise normal rats caused a more than twofold increase in TGF-beta excretion without changes in systolic pressure or evidence of kidney damage. Concurrent treatment with amiloride did not alter this effect, indicating that aldosterone's stimulation of TGF-beta was independent of its regulation of sodium or potassium transport. However, concurrent treatment with spironolactone did block the increase in TGF-beta, indicating that the effect depends on the mineralocorticoid receptor. Renal mRNA for serum glucocorticoid kinase rose, but no change in TGF-beta message occurred, suggesting posttranscriptional enhancement of renal TGF-beta. In summary, aldosterone provokes renal TGF-beta, and this action may contribute to aldosterone's fibrotic propensity.</description><subject>Aldosterone - administration & dosage</subject><subject>Aldosterone - pharmacology</subject><subject>Aldosterone - urine</subject><subject>Angiotensin I - biosynthesis</subject><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>Body Weight - drug effects</subject><subject>Drug Implants</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Male</subject><subject>Nuclease Protection Assays</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renin - blood</subject><subject>Stimulation, Chemical</subject><subject>Transforming Growth Factor beta - biosynthesis</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Transforming Growth Factor beta - urine</subject><subject>Water-Electrolyte Balance - drug effects</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkF1LwzAUhoMobk5_gSC98q7znGRt0xtBxvyAgTcK3oW0PZkbbTOTFPHfm32IV-eF9wPOw9g1whQx43d6s3XU63YKwIFPOYA4YePo8BRneX4adSkwlVnxMWIX3m8AAJHjORthhgJkWYzZ_cIYqkNiTaLbxvpAzvaU2D7ZbyfB6d4b67p1v0pWzn6Hz8ToOliXVhT0JTszuvV0dbwT9v64eJs_p8vXp5f5wzKtBWBIMylLnWPT6KowUedakoZZTk1dFBKFyHidR4u4pNxU2MBMGjBVA6YQpkQxYbeH3a2zXwP5oLq1r6ltdU928KrAMr4GMgbFIVg7670jo7Zu3Wn3oxDUDpv6w6b22NQOW2zdHOeHqqPmv3PkJH4BrTxrPQ</recordid><startdate>200406</startdate><enddate>200406</enddate><creator>Juknevicius, Irmantas</creator><creator>Segal, Yoav</creator><creator>Kren, Stefan</creator><creator>Lee, Rutha</creator><creator>Hostetter, Thomas H</creator><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>200406</creationdate><title>Effect of aldosterone on renal transforming growth factor-beta</title><author>Juknevicius, Irmantas ; Segal, Yoav ; Kren, Stefan ; Lee, Rutha ; Hostetter, Thomas H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c301t-5889a61ddab7f8896a8ea046edc77813352c6b7fe28e6fb1d048f0fbd0f73f913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Aldosterone - administration & dosage</topic><topic>Aldosterone - pharmacology</topic><topic>Aldosterone - urine</topic><topic>Angiotensin I - biosynthesis</topic><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>Body Weight - drug effects</topic><topic>Drug Implants</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Male</topic><topic>Nuclease Protection Assays</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renin - blood</topic><topic>Stimulation, Chemical</topic><topic>Transforming Growth Factor beta - biosynthesis</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Transforming Growth Factor beta - urine</topic><topic>Water-Electrolyte Balance - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Juknevicius, Irmantas</creatorcontrib><creatorcontrib>Segal, Yoav</creatorcontrib><creatorcontrib>Kren, Stefan</creatorcontrib><creatorcontrib>Lee, Rutha</creatorcontrib><creatorcontrib>Hostetter, Thomas H</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>Juknevicius, Irmantas</au><au>Segal, Yoav</au><au>Kren, Stefan</au><au>Lee, Rutha</au><au>Hostetter, Thomas H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of aldosterone on renal transforming growth factor-beta</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2004-06</date><risdate>2004</risdate><volume>286</volume><issue>6</issue><spage>F1059</spage><epage>F1062</epage><pages>F1059-F1062</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>Aldosterone participates in the pathophysiology of several models of progressive chronic renal disease. Because of the causal connection between transforming growth factor-beta(1) (TGF-beta) and scarring in many such models, we hypothesized that aldosterone could evoke TGF-beta in the kidney. Aldosterone infusion for 3 days in otherwise normal rats caused a more than twofold increase in TGF-beta excretion without changes in systolic pressure or evidence of kidney damage. Concurrent treatment with amiloride did not alter this effect, indicating that aldosterone's stimulation of TGF-beta was independent of its regulation of sodium or potassium transport. However, concurrent treatment with spironolactone did block the increase in TGF-beta, indicating that the effect depends on the mineralocorticoid receptor. Renal mRNA for serum glucocorticoid kinase rose, but no change in TGF-beta message occurred, suggesting posttranscriptional enhancement of renal TGF-beta. In summary, aldosterone provokes renal TGF-beta, and this action may contribute to aldosterone's fibrotic propensity.</abstract><cop>United States</cop><pmid>15130897</pmid><doi>10.1152/ajprenal.00202.2003</doi></addata></record> |
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| identifier | ISSN: 1931-857X |
| ispartof | American journal of physiology. Renal physiology, 2004-06, Vol.286 (6), p.F1059-F1062 |
| issn | 1931-857X 1522-1466 |
| language | eng |
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| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals |
| subjects | Aldosterone - administration & dosage Aldosterone - pharmacology Aldosterone - urine Angiotensin I - biosynthesis Animals Blood Pressure - drug effects Body Weight - drug effects Drug Implants Gene Expression Regulation - drug effects Kidney - drug effects Kidney - metabolism Male Nuclease Protection Assays Rats Rats, Sprague-Dawley Renin - blood Stimulation, Chemical Transforming Growth Factor beta - biosynthesis Transforming Growth Factor beta - genetics Transforming Growth Factor beta - urine Water-Electrolyte Balance - drug effects |
| title | Effect of aldosterone on renal transforming growth factor-beta |
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