Prevention of Renal Damage by Angiotensin II Blockade, Accompanied by Increased Renal Hepatocyte Growth Factor in Experimental Hypertensive Rats
Hepatocyte growth factor (HGF) is a unique growth factor that has many protective functions against renal damage. Our previous study demonstrated that HGF stimulated the growth of endothelial and epithelial cells without the replication of mesangial cells. Moreover, angiotensin (Ang) II significantl...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 1999-08, Vol.34 (2), p.279-284 |
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| creator | Matsumoto, Keiko Morishita, Ryuichi Moriguchi, Atsushi Tomita, Naruya Yo, Yoshikage Nishii, Tadahiko Matsumoto, Kunio Nakamura, Toshikazu Higaki, Jitsuo Ogihara, Toshio |
| description | Hepatocyte growth factor (HGF) is a unique growth factor that has many protective functions against renal damage. Our previous study demonstrated that HGF stimulated the growth of endothelial and epithelial cells without the replication of mesangial cells. Moreover, angiotensin (Ang) II significantly decreased local HGF production in mesangial cells. Therefore, we examined the effects of Ang II blockade on renal HGF expression and renal damage in experimental hypertensive rats. An angiotensin-converting enzyme inhibitor (cilazapril; 10 mg [middle dot] kg [middle dot] d), an Ang II type 1 receptor antagonist (E-4177; 30 mg [middle dot] kg [middle dot] d), hydralazine (8 mg [middle dot] kg [middle dot] d), and vehicle were administered to 16-week-old stroke-prone spontaneously hypertensive rats (SHR-SP) for 3 weeks. Renal damage was evaluated with a computer analysis system, and renal HGF mRNA was measured by Northern blot analysis. Blood pressure of SHR-SP was significantly decreased by all drug treatments compared with vehicle. Moreover, cilazapril, E-4177, and hydralazine significantly decreased the thickening and necrosis of blood vessels compared with vehicle. Similarly, degeneration and necrosis of glomeruli were also markedly improved by cilazapril and E-4177 (P |
| doi_str_mv | 10.1161/01.hyp.34.2.279 |
| format | Article |
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Our previous study demonstrated that HGF stimulated the growth of endothelial and epithelial cells without the replication of mesangial cells. Moreover, angiotensin (Ang) II significantly decreased local HGF production in mesangial cells. Therefore, we examined the effects of Ang II blockade on renal HGF expression and renal damage in experimental hypertensive rats. An angiotensin-converting enzyme inhibitor (cilazapril; 10 mg [middle dot] kg [middle dot] d), an Ang II type 1 receptor antagonist (E-4177; 30 mg [middle dot] kg [middle dot] d), hydralazine (8 mg [middle dot] kg [middle dot] d), and vehicle were administered to 16-week-old stroke-prone spontaneously hypertensive rats (SHR-SP) for 3 weeks. Renal damage was evaluated with a computer analysis system, and renal HGF mRNA was measured by Northern blot analysis. Blood pressure of SHR-SP was significantly decreased by all drug treatments compared with vehicle. Moreover, cilazapril, E-4177, and hydralazine significantly decreased the thickening and necrosis of blood vessels compared with vehicle. Similarly, degeneration and necrosis of glomeruli were also markedly improved by cilazapril and E-4177 (P<0.01). We next examined the effects of Ang II blockade on renal HGF expression in SHR-SP. Renal HGF mRNA was markedly decreased in SHR-SP compared with Wistar-Kyoto rats, although Ang II blockade by cilazapril and E-4177 but not hydralazine significantly increased renal HGF mRNA in SHR-SP. Ang II blockade significantly increased renal HGF (a protective growth factor for tubular epithelial cells); thus, we examined tubular histological appearance. Degeneration and necrosis of tubules were significantly improved by cilazapril and E-4177 treatment (P<0.01). In addition, cell infiltration into the glomeruli and hemorrhage were also significantly reduced in SHR-SP treated with cilazapril or E-4177. The present data demonstrated the prevention of renal damage by Ang II blockade in SHR-SP, which was accompanied by a significant increase in renal HGF mRNA. Given the strong mitogenic activity and antiapoptotic actions of HGF on endothelial and epithelial cells, we believe that increased local HGF production by the blockade of Ang II may improve renal function in hypertension. (Hypertension. 1999;34:279-284.)</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.34.2.279</identifier><identifier>PMID: 10454454</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Angiotensin II - antagonists & inhibitors ; Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Animals ; Antihypertensive agents ; Antihypertensive Agents - pharmacology ; Antihypertensive Agents - therapeutic use ; Biological and medical sciences ; Blood Pressure - drug effects ; Blotting, Northern ; Cardiovascular system ; Cilazapril - pharmacology ; Cilazapril - therapeutic use ; Data Interpretation, Statistical ; Hepatocyte Growth Factor - biosynthesis ; Hepatocyte Growth Factor - genetics ; Hydralazine - pharmacology ; Hydralazine - therapeutic use ; Hypertension, Renal - pathology ; Hypertension, Renal - prevention & control ; Imidazoles - pharmacology ; Imidazoles - therapeutic use ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Kidney Tubules - drug effects ; Male ; Medical sciences ; Pharmacology. Drug treatments ; Pyridines - pharmacology ; Pyridines - therapeutic use ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; RNA, Messenger - analysis ; Time Factors</subject><ispartof>Hypertension (Dallas, Tex. 1979), 1999-08, Vol.34 (2), p.279-284</ispartof><rights>1999 American Heart Association, Inc.</rights><rights>1999 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Aug 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5422-5f2480c466529c94bac5daae333bfe0fe758691153f6c18a6360e35423cfb1853</citedby><cites>FETCH-LOGICAL-c5422-5f2480c466529c94bac5daae333bfe0fe758691153f6c18a6360e35423cfb1853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,777,781,786,787,3674,23911,23912,25121,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1950196$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10454454$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsumoto, Keiko</creatorcontrib><creatorcontrib>Morishita, Ryuichi</creatorcontrib><creatorcontrib>Moriguchi, Atsushi</creatorcontrib><creatorcontrib>Tomita, Naruya</creatorcontrib><creatorcontrib>Yo, Yoshikage</creatorcontrib><creatorcontrib>Nishii, Tadahiko</creatorcontrib><creatorcontrib>Matsumoto, Kunio</creatorcontrib><creatorcontrib>Nakamura, Toshikazu</creatorcontrib><creatorcontrib>Higaki, Jitsuo</creatorcontrib><creatorcontrib>Ogihara, Toshio</creatorcontrib><title>Prevention of Renal Damage by Angiotensin II Blockade, Accompanied by Increased Renal Hepatocyte Growth Factor in Experimental Hypertensive Rats</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Hepatocyte growth factor (HGF) is a unique growth factor that has many protective functions against renal damage. Our previous study demonstrated that HGF stimulated the growth of endothelial and epithelial cells without the replication of mesangial cells. Moreover, angiotensin (Ang) II significantly decreased local HGF production in mesangial cells. Therefore, we examined the effects of Ang II blockade on renal HGF expression and renal damage in experimental hypertensive rats. An angiotensin-converting enzyme inhibitor (cilazapril; 10 mg [middle dot] kg [middle dot] d), an Ang II type 1 receptor antagonist (E-4177; 30 mg [middle dot] kg [middle dot] d), hydralazine (8 mg [middle dot] kg [middle dot] d), and vehicle were administered to 16-week-old stroke-prone spontaneously hypertensive rats (SHR-SP) for 3 weeks. Renal damage was evaluated with a computer analysis system, and renal HGF mRNA was measured by Northern blot analysis. Blood pressure of SHR-SP was significantly decreased by all drug treatments compared with vehicle. Moreover, cilazapril, E-4177, and hydralazine significantly decreased the thickening and necrosis of blood vessels compared with vehicle. Similarly, degeneration and necrosis of glomeruli were also markedly improved by cilazapril and E-4177 (P<0.01). We next examined the effects of Ang II blockade on renal HGF expression in SHR-SP. Renal HGF mRNA was markedly decreased in SHR-SP compared with Wistar-Kyoto rats, although Ang II blockade by cilazapril and E-4177 but not hydralazine significantly increased renal HGF mRNA in SHR-SP. Ang II blockade significantly increased renal HGF (a protective growth factor for tubular epithelial cells); thus, we examined tubular histological appearance. Degeneration and necrosis of tubules were significantly improved by cilazapril and E-4177 treatment (P<0.01). In addition, cell infiltration into the glomeruli and hemorrhage were also significantly reduced in SHR-SP treated with cilazapril or E-4177. The present data demonstrated the prevention of renal damage by Ang II blockade in SHR-SP, which was accompanied by a significant increase in renal HGF mRNA. Given the strong mitogenic activity and antiapoptotic actions of HGF on endothelial and epithelial cells, we believe that increased local HGF production by the blockade of Ang II may improve renal function in hypertension. (Hypertension. 1999;34:279-284.)</description><subject>Angiotensin II - antagonists & inhibitors</subject><subject>Angiotensin Receptor Antagonists</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Animals</subject><subject>Antihypertensive agents</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Blotting, Northern</subject><subject>Cardiovascular system</subject><subject>Cilazapril - pharmacology</subject><subject>Cilazapril - therapeutic use</subject><subject>Data Interpretation, Statistical</subject><subject>Hepatocyte Growth Factor - biosynthesis</subject><subject>Hepatocyte Growth Factor - genetics</subject><subject>Hydralazine - pharmacology</subject><subject>Hydralazine - therapeutic use</subject><subject>Hypertension, Renal - pathology</subject><subject>Hypertension, Renal - prevention & control</subject><subject>Imidazoles - pharmacology</subject><subject>Imidazoles - therapeutic use</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Tubules - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Pyridines - pharmacology</subject><subject>Pyridines - therapeutic use</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>RNA, Messenger - analysis</subject><subject>Time Factors</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkV-L1DAUxYMo7rj67JsEEZ9sN__bPI7r7s7AgsuioE8hzdzudLfT1KTdsd_Cj2zGDiiGhHDgd8_lcBB6TUlOqaJnhObbqc-5yFnOCv0ELahkIhNS8adoQagWmab02wl6EeM9IVQIUTxHJ5QIKdJdoF83AR6hGxrfYV_jW-hsiz_Znb0DXE142d01foAuNh1er_HH1rsHu4EPeOmc3_W2a2Bz4NadC2BjErPDCno7eDcNgK-C3w9bfGnd4ANOPhc_ewjNLi09gFMSfxY8Ar61Q3yJntW2jfDq-J-ir5cXX85X2fXnq_X58jpzUjCWyZqJkjihlGTaaVFZJzfWAue8qoHUUMhSpeiS18rR0iquCPA0yl1d0VLyU_R-9u2D_zFCHMyuiQ7a1nbgx2iU1qUoiyKBb_8D7_0YUshoGJGsUJQf3M5myAUfY4Da9CmiDZOhxByaMoSa1fcbw4VhJjWVJt4cbcdqB5t_-LmaBLw7AjY629bBdq6JfzktU70qYWLG9r4dIMSHdtxDMFuw7bA1JB3BVJlRrTUpk8rSY4z_BrXTq7k</recordid><startdate>199908</startdate><enddate>199908</enddate><creator>Matsumoto, Keiko</creator><creator>Morishita, Ryuichi</creator><creator>Moriguchi, Atsushi</creator><creator>Tomita, Naruya</creator><creator>Yo, Yoshikage</creator><creator>Nishii, Tadahiko</creator><creator>Matsumoto, Kunio</creator><creator>Nakamura, Toshikazu</creator><creator>Higaki, Jitsuo</creator><creator>Ogihara, Toshio</creator><general>American Heart Association, Inc</general><general>Lippincott</general><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>K9.</scope><scope>7X8</scope></search><sort><creationdate>199908</creationdate><title>Prevention of Renal Damage by Angiotensin II Blockade, Accompanied by Increased Renal Hepatocyte Growth Factor in Experimental Hypertensive Rats</title><author>Matsumoto, Keiko ; Morishita, Ryuichi ; Moriguchi, Atsushi ; Tomita, Naruya ; Yo, Yoshikage ; Nishii, Tadahiko ; Matsumoto, Kunio ; Nakamura, Toshikazu ; Higaki, Jitsuo ; Ogihara, Toshio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5422-5f2480c466529c94bac5daae333bfe0fe758691153f6c18a6360e35423cfb1853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Angiotensin II - antagonists & inhibitors</topic><topic>Angiotensin Receptor Antagonists</topic><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</topic><topic>Animals</topic><topic>Antihypertensive agents</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Blotting, Northern</topic><topic>Cardiovascular system</topic><topic>Cilazapril - pharmacology</topic><topic>Cilazapril - therapeutic use</topic><topic>Data Interpretation, Statistical</topic><topic>Hepatocyte Growth Factor - biosynthesis</topic><topic>Hepatocyte Growth Factor - genetics</topic><topic>Hydralazine - pharmacology</topic><topic>Hydralazine - therapeutic use</topic><topic>Hypertension, Renal - pathology</topic><topic>Hypertension, Renal - prevention & control</topic><topic>Imidazoles - pharmacology</topic><topic>Imidazoles - therapeutic use</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Tubules - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Pyridines - pharmacology</topic><topic>Pyridines - therapeutic use</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>RNA, Messenger - analysis</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsumoto, Keiko</creatorcontrib><creatorcontrib>Morishita, Ryuichi</creatorcontrib><creatorcontrib>Moriguchi, Atsushi</creatorcontrib><creatorcontrib>Tomita, Naruya</creatorcontrib><creatorcontrib>Yo, Yoshikage</creatorcontrib><creatorcontrib>Nishii, Tadahiko</creatorcontrib><creatorcontrib>Matsumoto, Kunio</creatorcontrib><creatorcontrib>Nakamura, Toshikazu</creatorcontrib><creatorcontrib>Higaki, Jitsuo</creatorcontrib><creatorcontrib>Ogihara, Toshio</creatorcontrib><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 Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsumoto, Keiko</au><au>Morishita, Ryuichi</au><au>Moriguchi, Atsushi</au><au>Tomita, Naruya</au><au>Yo, Yoshikage</au><au>Nishii, Tadahiko</au><au>Matsumoto, Kunio</au><au>Nakamura, Toshikazu</au><au>Higaki, Jitsuo</au><au>Ogihara, Toshio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prevention of Renal Damage by Angiotensin II Blockade, Accompanied by Increased Renal Hepatocyte Growth Factor in Experimental Hypertensive Rats</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>1999-08</date><risdate>1999</risdate><volume>34</volume><issue>2</issue><spage>279</spage><epage>284</epage><pages>279-284</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Hepatocyte growth factor (HGF) is a unique growth factor that has many protective functions against renal damage. Our previous study demonstrated that HGF stimulated the growth of endothelial and epithelial cells without the replication of mesangial cells. Moreover, angiotensin (Ang) II significantly decreased local HGF production in mesangial cells. Therefore, we examined the effects of Ang II blockade on renal HGF expression and renal damage in experimental hypertensive rats. An angiotensin-converting enzyme inhibitor (cilazapril; 10 mg [middle dot] kg [middle dot] d), an Ang II type 1 receptor antagonist (E-4177; 30 mg [middle dot] kg [middle dot] d), hydralazine (8 mg [middle dot] kg [middle dot] d), and vehicle were administered to 16-week-old stroke-prone spontaneously hypertensive rats (SHR-SP) for 3 weeks. Renal damage was evaluated with a computer analysis system, and renal HGF mRNA was measured by Northern blot analysis. Blood pressure of SHR-SP was significantly decreased by all drug treatments compared with vehicle. Moreover, cilazapril, E-4177, and hydralazine significantly decreased the thickening and necrosis of blood vessels compared with vehicle. Similarly, degeneration and necrosis of glomeruli were also markedly improved by cilazapril and E-4177 (P<0.01). We next examined the effects of Ang II blockade on renal HGF expression in SHR-SP. Renal HGF mRNA was markedly decreased in SHR-SP compared with Wistar-Kyoto rats, although Ang II blockade by cilazapril and E-4177 but not hydralazine significantly increased renal HGF mRNA in SHR-SP. Ang II blockade significantly increased renal HGF (a protective growth factor for tubular epithelial cells); thus, we examined tubular histological appearance. Degeneration and necrosis of tubules were significantly improved by cilazapril and E-4177 treatment (P<0.01). In addition, cell infiltration into the glomeruli and hemorrhage were also significantly reduced in SHR-SP treated with cilazapril or E-4177. The present data demonstrated the prevention of renal damage by Ang II blockade in SHR-SP, which was accompanied by a significant increase in renal HGF mRNA. Given the strong mitogenic activity and antiapoptotic actions of HGF on endothelial and epithelial cells, we believe that increased local HGF production by the blockade of Ang II may improve renal function in hypertension. (Hypertension. 1999;34:279-284.)</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>10454454</pmid><doi>10.1161/01.hyp.34.2.279</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 1999-08, Vol.34 (2), p.279-284 |
| issn | 0194-911X 1524-4563 |
| language | eng |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Ovid Autoload |
| subjects | Angiotensin II - antagonists & inhibitors Angiotensin Receptor Antagonists Angiotensin-Converting Enzyme Inhibitors - pharmacology Angiotensin-Converting Enzyme Inhibitors - therapeutic use Animals Antihypertensive agents Antihypertensive Agents - pharmacology Antihypertensive Agents - therapeutic use Biological and medical sciences Blood Pressure - drug effects Blotting, Northern Cardiovascular system Cilazapril - pharmacology Cilazapril - therapeutic use Data Interpretation, Statistical Hepatocyte Growth Factor - biosynthesis Hepatocyte Growth Factor - genetics Hydralazine - pharmacology Hydralazine - therapeutic use Hypertension, Renal - pathology Hypertension, Renal - prevention & control Imidazoles - pharmacology Imidazoles - therapeutic use Kidney - drug effects Kidney - metabolism Kidney - pathology Kidney Tubules - drug effects Male Medical sciences Pharmacology. Drug treatments Pyridines - pharmacology Pyridines - therapeutic use Rats Rats, Inbred SHR Rats, Inbred WKY RNA, Messenger - analysis Time Factors |
| title | Prevention of Renal Damage by Angiotensin II Blockade, Accompanied by Increased Renal Hepatocyte Growth Factor in Experimental Hypertensive Rats |
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