Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism
Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we ex...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 2002-06, Vol.282 (6), p.F991-F997 |
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| container_title | American journal of physiology. Renal physiology |
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| creator | Mazzali, Marilda Kanellis, John Han, Lin Feng, Lili Xia, Yi-Yang Chen, Qiang Kang, Duk-Hee Gordon, Katherine L Watanabe, Susumu Nakagawa, Takahiko Lan, Hui Y Johnson, Richard J |
| description | Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature. Rats fed 2% oxonic acid and a low-salt diet for 7 wk developed mild hyperuricemia (1.8 vs. 1.4 mg/dl, P < 0.05), hypertension [147 vs. 127 mmHg systolic blood pressure (SBP), P < 0.05], and afferent arteriolar thickening, with a 35% increase in medial area (P < 0.05). Allopurinol or benziodarone prevented the hyperuricemia, hypertension, and arteriolopathy. Hydrochlorothiazide treatment did not prevent the hyperuricemia or arteriolopathy despite controlling blood pressure. In contrast, the arteriolopathy and hypertension were prevented by both enalapril and losartan. Uric acid also directly stimulated vascular smooth muscle cell proliferation in vitro, and this was partially inhibited by losartan. Thus hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system. |
| doi_str_mv | 10.1152/ajprenal.00283.2001 |
| format | Article |
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We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature. Rats fed 2% oxonic acid and a low-salt diet for 7 wk developed mild hyperuricemia (1.8 vs. 1.4 mg/dl, P < 0.05), hypertension [147 vs. 127 mmHg systolic blood pressure (SBP), P < 0.05], and afferent arteriolar thickening, with a 35% increase in medial area (P < 0.05). Allopurinol or benziodarone prevented the hyperuricemia, hypertension, and arteriolopathy. Hydrochlorothiazide treatment did not prevent the hyperuricemia or arteriolopathy despite controlling blood pressure. In contrast, the arteriolopathy and hypertension were prevented by both enalapril and losartan. Uric acid also directly stimulated vascular smooth muscle cell proliferation in vitro, and this was partially inhibited by losartan. Thus hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00283.2001</identifier><identifier>PMID: 11997315</identifier><language>eng</language><publisher>United States</publisher><subject>Administration, Oral ; Allopurinol - pharmacology ; Angiotensin II - metabolism ; Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Animals ; Arterioles - drug effects ; Arterioles - pathology ; Benzofurans - pharmacology ; Blood Pressure - drug effects ; Diuretics ; Enalapril - pharmacology ; Hydrochlorothiazide - pharmacology ; Hypertension - chemically induced ; Hypertension - pathology ; Hypertension - prevention & control ; Kidney - blood supply ; Kidney - pathology ; Losartan - pharmacology ; Male ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - pathology ; Oxonic Acid ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride Symporter Inhibitors - pharmacology ; Sodium Chloride, Dietary ; Uric Acid - blood ; Uric Acid - pharmacology ; Uricosuric Agents - pharmacology ; Vascular Diseases - chemically induced ; Vascular Diseases - pathology ; Vascular Diseases - prevention & control</subject><ispartof>American journal of physiology. Renal physiology, 2002-06, Vol.282 (6), p.F991-F997</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-1e63fd6cbe319c41db427c86d7de6a66fea10996bff9cafecc9958be198e75e13</citedby><cites>FETCH-LOGICAL-c372t-1e63fd6cbe319c41db427c86d7de6a66fea10996bff9cafecc9958be198e75e13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11997315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mazzali, Marilda</creatorcontrib><creatorcontrib>Kanellis, John</creatorcontrib><creatorcontrib>Han, Lin</creatorcontrib><creatorcontrib>Feng, Lili</creatorcontrib><creatorcontrib>Xia, Yi-Yang</creatorcontrib><creatorcontrib>Chen, Qiang</creatorcontrib><creatorcontrib>Kang, Duk-Hee</creatorcontrib><creatorcontrib>Gordon, Katherine L</creatorcontrib><creatorcontrib>Watanabe, Susumu</creatorcontrib><creatorcontrib>Nakagawa, Takahiko</creatorcontrib><creatorcontrib>Lan, Hui Y</creatorcontrib><creatorcontrib>Johnson, Richard J</creatorcontrib><title>Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature. Rats fed 2% oxonic acid and a low-salt diet for 7 wk developed mild hyperuricemia (1.8 vs. 1.4 mg/dl, P < 0.05), hypertension [147 vs. 127 mmHg systolic blood pressure (SBP), P < 0.05], and afferent arteriolar thickening, with a 35% increase in medial area (P < 0.05). Allopurinol or benziodarone prevented the hyperuricemia, hypertension, and arteriolopathy. Hydrochlorothiazide treatment did not prevent the hyperuricemia or arteriolopathy despite controlling blood pressure. In contrast, the arteriolopathy and hypertension were prevented by both enalapril and losartan. Uric acid also directly stimulated vascular smooth muscle cell proliferation in vitro, and this was partially inhibited by losartan. Thus hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system.</description><subject>Administration, Oral</subject><subject>Allopurinol - pharmacology</subject><subject>Angiotensin II - metabolism</subject><subject>Angiotensin Receptor Antagonists</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Arterioles - drug effects</subject><subject>Arterioles - pathology</subject><subject>Benzofurans - pharmacology</subject><subject>Blood Pressure - drug effects</subject><subject>Diuretics</subject><subject>Enalapril - pharmacology</subject><subject>Hydrochlorothiazide - pharmacology</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - pathology</subject><subject>Hypertension - prevention & control</subject><subject>Kidney - blood supply</subject><subject>Kidney - pathology</subject><subject>Losartan - pharmacology</subject><subject>Male</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Oxonic Acid</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sodium Chloride Symporter Inhibitors - pharmacology</subject><subject>Sodium Chloride, Dietary</subject><subject>Uric Acid - blood</subject><subject>Uric Acid - pharmacology</subject><subject>Uricosuric Agents - pharmacology</subject><subject>Vascular Diseases - chemically induced</subject><subject>Vascular Diseases - pathology</subject><subject>Vascular Diseases - prevention & control</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN1KxDAQhYMo7rr6BILkBVozyTZtLmVRV1jwRsG7kqQTtkv_SNqLvr3ZH_FmZmDOOcN8hDwCSwEy_qwPg8dONyljvBApZwyuyDJueAJrKa_jrAQkRZb_LMhdCAcWFcDhliwAlMoFZEvitvOAfvK1xbbWtO6qyWKgmg6-brWf6ekE1X5EX_dNP-hxP0cZ9XoM1MxRaZq-r6IeQ5g8JjECB4ylG2mLdq-7OrT35MbpJuDDpa_I99vr12ab7D7fPzYvu8SKnI8JoBSuktagAGXXUJk1z20hq7xCqaV0qIEpJY1zymqH1iqVFQZBFZhnCGJFxDnX-j4Ej668_FECK4_Uyj9q5YlaeaQWXU9n1zCZFqt_zwWT-AXQXG5g</recordid><startdate>200206</startdate><enddate>200206</enddate><creator>Mazzali, Marilda</creator><creator>Kanellis, John</creator><creator>Han, Lin</creator><creator>Feng, Lili</creator><creator>Xia, Yi-Yang</creator><creator>Chen, Qiang</creator><creator>Kang, Duk-Hee</creator><creator>Gordon, Katherine L</creator><creator>Watanabe, Susumu</creator><creator>Nakagawa, Takahiko</creator><creator>Lan, Hui Y</creator><creator>Johnson, Richard J</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></search><sort><creationdate>200206</creationdate><title>Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism</title><author>Mazzali, Marilda ; Kanellis, John ; Han, Lin ; Feng, Lili ; Xia, Yi-Yang ; Chen, Qiang ; Kang, Duk-Hee ; Gordon, Katherine L ; Watanabe, Susumu ; Nakagawa, Takahiko ; Lan, Hui Y ; Johnson, Richard J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-1e63fd6cbe319c41db427c86d7de6a66fea10996bff9cafecc9958be198e75e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Administration, Oral</topic><topic>Allopurinol - pharmacology</topic><topic>Angiotensin II - metabolism</topic><topic>Angiotensin Receptor Antagonists</topic><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Arterioles - drug effects</topic><topic>Arterioles - pathology</topic><topic>Benzofurans - pharmacology</topic><topic>Blood Pressure - drug effects</topic><topic>Diuretics</topic><topic>Enalapril - pharmacology</topic><topic>Hydrochlorothiazide - pharmacology</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - pathology</topic><topic>Hypertension - prevention & control</topic><topic>Kidney - blood supply</topic><topic>Kidney - pathology</topic><topic>Losartan - pharmacology</topic><topic>Male</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Oxonic Acid</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sodium Chloride Symporter Inhibitors - pharmacology</topic><topic>Sodium Chloride, Dietary</topic><topic>Uric Acid - blood</topic><topic>Uric Acid - pharmacology</topic><topic>Uricosuric Agents - pharmacology</topic><topic>Vascular Diseases - chemically induced</topic><topic>Vascular Diseases - pathology</topic><topic>Vascular Diseases - prevention & control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mazzali, Marilda</creatorcontrib><creatorcontrib>Kanellis, John</creatorcontrib><creatorcontrib>Han, Lin</creatorcontrib><creatorcontrib>Feng, Lili</creatorcontrib><creatorcontrib>Xia, Yi-Yang</creatorcontrib><creatorcontrib>Chen, Qiang</creatorcontrib><creatorcontrib>Kang, Duk-Hee</creatorcontrib><creatorcontrib>Gordon, Katherine L</creatorcontrib><creatorcontrib>Watanabe, Susumu</creatorcontrib><creatorcontrib>Nakagawa, Takahiko</creatorcontrib><creatorcontrib>Lan, Hui Y</creatorcontrib><creatorcontrib>Johnson, Richard J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mazzali, Marilda</au><au>Kanellis, John</au><au>Han, Lin</au><au>Feng, Lili</au><au>Xia, Yi-Yang</au><au>Chen, Qiang</au><au>Kang, Duk-Hee</au><au>Gordon, Katherine L</au><au>Watanabe, Susumu</au><au>Nakagawa, Takahiko</au><au>Lan, Hui Y</au><au>Johnson, Richard J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2002-06</date><risdate>2002</risdate><volume>282</volume><issue>6</issue><spage>F991</spage><epage>F997</epage><pages>F991-F997</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature. Rats fed 2% oxonic acid and a low-salt diet for 7 wk developed mild hyperuricemia (1.8 vs. 1.4 mg/dl, P < 0.05), hypertension [147 vs. 127 mmHg systolic blood pressure (SBP), P < 0.05], and afferent arteriolar thickening, with a 35% increase in medial area (P < 0.05). Allopurinol or benziodarone prevented the hyperuricemia, hypertension, and arteriolopathy. Hydrochlorothiazide treatment did not prevent the hyperuricemia or arteriolopathy despite controlling blood pressure. In contrast, the arteriolopathy and hypertension were prevented by both enalapril and losartan. Uric acid also directly stimulated vascular smooth muscle cell proliferation in vitro, and this was partially inhibited by losartan. Thus hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system.</abstract><cop>United States</cop><pmid>11997315</pmid><doi>10.1152/ajprenal.00283.2001</doi></addata></record> |
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| identifier | ISSN: 1931-857X |
| ispartof | American journal of physiology. Renal physiology, 2002-06, Vol.282 (6), p.F991-F997 |
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| subjects | Administration, Oral Allopurinol - pharmacology Angiotensin II - metabolism Angiotensin Receptor Antagonists Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Arterioles - drug effects Arterioles - pathology Benzofurans - pharmacology Blood Pressure - drug effects Diuretics Enalapril - pharmacology Hydrochlorothiazide - pharmacology Hypertension - chemically induced Hypertension - pathology Hypertension - prevention & control Kidney - blood supply Kidney - pathology Losartan - pharmacology Male Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - pathology Oxonic Acid Rats Rats, Sprague-Dawley Sodium Chloride Symporter Inhibitors - pharmacology Sodium Chloride, Dietary Uric Acid - blood Uric Acid - pharmacology Uricosuric Agents - pharmacology Vascular Diseases - chemically induced Vascular Diseases - pathology Vascular Diseases - prevention & control |
| title | Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism |
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