Inhibition of prolyl hydroxylase domain-containing protein on hypertension/renal injury induced by high salt diet and nitric oxide withdrawal
Nitric oxide just as prolyl hydroxylase domain-containing protein (PHD) is a regulator of hypoxia inducible factor-1 α (HIF-1α), a transcription factor complex that controls the expression of most genes involved in hypoxia and cardiovascular diseases. In the absence of nitric oxide, it is not clear...
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| Veröffentlicht in: | Journal of hypertension 2013-10, Vol.31 (10), p.2043-2049 |
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| creator | Dallatu, Mohammad K Choi, Myung Oyekan, Adebayo O |
| description | Nitric oxide just as prolyl hydroxylase domain-containing protein (PHD) is a regulator of hypoxia inducible factor-1 α (HIF-1α), a transcription factor complex that controls the expression of most genes involved in hypoxia and cardiovascular diseases. In the absence of nitric oxide, it is not clear how HIF-1α and PHD are regulated and to what extent they contribute to the ensuing disorder.
Using the nitric oxide withdrawal/high salt diet model of hypertensive renal injury, this study tested the hypothesis that removal of the inhibition by nitric oxide on PHD predisposes to increased PHD but reduced HIF-1α expression, hypertension and renal injury.
In animals treated with N-nitro-L-arginine (L-NNA; 250 mg/l in drinking water for 14 days) and high salt diet (4% NaCl), there was hypertension (41±5%, P |
| doi_str_mv | 10.1097/HJH.0b013e32836356a0 |
| format | Article |
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Using the nitric oxide withdrawal/high salt diet model of hypertensive renal injury, this study tested the hypothesis that removal of the inhibition by nitric oxide on PHD predisposes to increased PHD but reduced HIF-1α expression, hypertension and renal injury.
In animals treated with N-nitro-L-arginine (L-NNA; 250 mg/l in drinking water for 14 days) and high salt diet (4% NaCl), there was hypertension (41±5%, P<0.05), proteinuria (three-fold, P<0.05), kidney (22±3%, P<0.05) and heart enlargement (24±3%, P<0.05), as well as increased renal osteopontin (21±3%, P<0.05) and collagen IV (24±4%, P<0.05) expression. Accompanying these effects were increased expression of PHD1 (24±4%, P<0.05) and PHD2 (36±4%, P<0.05) but reduced HIF-1α (35±6%, P < 0.05) expression. Dimethyloxallyl glycine (5mg/kg), a PHD inhibitor, paradoxically exacerbated hypertension (46±7%, P<0.05), proteinuria (two-fold, P <0.05), and increased osteopontin (15±2%, P<0.05) and HIF-1α (31±5%, P<0.05) expression with no change in PHD1/2 expression or kidney and heart enlargement.
These data suggest that the protective effect of physiological levels of nitric oxide may be by virtue of inhibition of PHD or increased HIF-1α expression, hence, the pathological changes produced following its withdrawal was accompanied by increased PHD or decreased HIF-1α expression. Exacerbation of hypertension and renal injury following PHD inhibition suggests a deleterious effect in the chronic setting and challenges the dogma that inhibition of PHD is useful in cardiovascular diseases.]]></description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/HJH.0b013e32836356a0</identifier><identifier>PMID: 23811999</identifier><language>eng</language><publisher>England</publisher><subject>Animals ; Blood Pressure ; Collagen Type IV - metabolism ; Female ; Gene Expression Regulation ; Hypertension - complications ; Hypertension - physiopathology ; Hypoxia - metabolism ; Hypoxia - pathology ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism ; Kidney - pathology ; Kidney Diseases - complications ; Kidney Diseases - metabolism ; Kidney Diseases - physiopathology ; Male ; Myocardium - pathology ; Nitric Oxide - physiology ; Nitric Oxide Synthase - antagonists & inhibitors ; Osteopontin - metabolism ; Oxidative Stress ; Protein Structure, Tertiary ; Proteinuria - complications ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride, Dietary - adverse effects</subject><ispartof>Journal of hypertension, 2013-10, Vol.31 (10), p.2043-2049</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-bbfe8b5afe8eb2cb3cb74800621fbbf5a6b40bf93963b86c4b751aadea8509543</citedby><cites>FETCH-LOGICAL-c373t-bbfe8b5afe8eb2cb3cb74800621fbbf5a6b40bf93963b86c4b751aadea8509543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23811999$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dallatu, Mohammad K</creatorcontrib><creatorcontrib>Choi, Myung</creatorcontrib><creatorcontrib>Oyekan, Adebayo O</creatorcontrib><title>Inhibition of prolyl hydroxylase domain-containing protein on hypertension/renal injury induced by high salt diet and nitric oxide withdrawal</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description><![CDATA[Nitric oxide just as prolyl hydroxylase domain-containing protein (PHD) is a regulator of hypoxia inducible factor-1 α (HIF-1α), a transcription factor complex that controls the expression of most genes involved in hypoxia and cardiovascular diseases. In the absence of nitric oxide, it is not clear how HIF-1α and PHD are regulated and to what extent they contribute to the ensuing disorder.
Using the nitric oxide withdrawal/high salt diet model of hypertensive renal injury, this study tested the hypothesis that removal of the inhibition by nitric oxide on PHD predisposes to increased PHD but reduced HIF-1α expression, hypertension and renal injury.
In animals treated with N-nitro-L-arginine (L-NNA; 250 mg/l in drinking water for 14 days) and high salt diet (4% NaCl), there was hypertension (41±5%, P<0.05), proteinuria (three-fold, P<0.05), kidney (22±3%, P<0.05) and heart enlargement (24±3%, P<0.05), as well as increased renal osteopontin (21±3%, P<0.05) and collagen IV (24±4%, P<0.05) expression. Accompanying these effects were increased expression of PHD1 (24±4%, P<0.05) and PHD2 (36±4%, P<0.05) but reduced HIF-1α (35±6%, P < 0.05) expression. Dimethyloxallyl glycine (5mg/kg), a PHD inhibitor, paradoxically exacerbated hypertension (46±7%, P<0.05), proteinuria (two-fold, P <0.05), and increased osteopontin (15±2%, P<0.05) and HIF-1α (31±5%, P<0.05) expression with no change in PHD1/2 expression or kidney and heart enlargement.
These data suggest that the protective effect of physiological levels of nitric oxide may be by virtue of inhibition of PHD or increased HIF-1α expression, hence, the pathological changes produced following its withdrawal was accompanied by increased PHD or decreased HIF-1α expression. Exacerbation of hypertension and renal injury following PHD inhibition suggests a deleterious effect in the chronic setting and challenges the dogma that inhibition of PHD is useful in cardiovascular diseases.]]></description><subject>Animals</subject><subject>Blood Pressure</subject><subject>Collagen Type IV - metabolism</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Hypertension - complications</subject><subject>Hypertension - physiopathology</subject><subject>Hypoxia - metabolism</subject><subject>Hypoxia - pathology</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - complications</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - physiopathology</subject><subject>Male</subject><subject>Myocardium - pathology</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Osteopontin - metabolism</subject><subject>Oxidative Stress</subject><subject>Protein Structure, Tertiary</subject><subject>Proteinuria - complications</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sodium Chloride, Dietary - adverse effects</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkctOHDEQRS0UBBPgD6LIy2x6sNvuh5fRKGFAI2UT1i0_qmkjjz2x3Rr6I_jneARkkU3dRZ1bpaqL0BdK1pSI7nb7sF0TRSgDVvesZU0ryRlaUd6xqmlE_wmtSN2yqnTqS_Q5pWdCSC86doEua9ZTKoRYodd7P1llsw0ehxEfYnCLw9NiYnhZnEyATdhL6ysdfC5q_dMJymAL7wt4gJjBp-K_jeClw9Y_z3EpYmYNBqsFT_Zpwkm6jI2FjKU32NscrcbhxRrAR5snE-VRumt0PkqX4OZdr9Djzx-_N9tq9-vufvN9V2nWsVwpNUKvGlkqqForplXHe0Lamo6l18hWcaJGwUTLVN9qrrqGSmlA9g0RDWdX6Nvb3HLKnxlSHvY2aXBOeghzGijnjNdUdCeUv6E6hpQijMMh2r2My0DJcApiKEEM_wdRbF_fN8xqD-af6ePz7C9vu4mU</recordid><startdate>20131001</startdate><enddate>20131001</enddate><creator>Dallatu, Mohammad K</creator><creator>Choi, Myung</creator><creator>Oyekan, Adebayo O</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>20131001</creationdate><title>Inhibition of prolyl hydroxylase domain-containing protein on hypertension/renal injury induced by high salt diet and nitric oxide withdrawal</title><author>Dallatu, Mohammad K ; Choi, Myung ; Oyekan, Adebayo O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c373t-bbfe8b5afe8eb2cb3cb74800621fbbf5a6b40bf93963b86c4b751aadea8509543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Blood Pressure</topic><topic>Collagen Type IV - metabolism</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Hypertension - complications</topic><topic>Hypertension - physiopathology</topic><topic>Hypoxia - metabolism</topic><topic>Hypoxia - pathology</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Diseases - complications</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - physiopathology</topic><topic>Male</topic><topic>Myocardium - pathology</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Osteopontin - metabolism</topic><topic>Oxidative Stress</topic><topic>Protein Structure, Tertiary</topic><topic>Proteinuria - complications</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sodium Chloride, Dietary - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dallatu, Mohammad K</creatorcontrib><creatorcontrib>Choi, Myung</creatorcontrib><creatorcontrib>Oyekan, Adebayo O</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>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dallatu, Mohammad K</au><au>Choi, Myung</au><au>Oyekan, Adebayo O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of prolyl hydroxylase domain-containing protein on hypertension/renal injury induced by high salt diet and nitric oxide withdrawal</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2013-10-01</date><risdate>2013</risdate><volume>31</volume><issue>10</issue><spage>2043</spage><epage>2049</epage><pages>2043-2049</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><abstract><![CDATA[Nitric oxide just as prolyl hydroxylase domain-containing protein (PHD) is a regulator of hypoxia inducible factor-1 α (HIF-1α), a transcription factor complex that controls the expression of most genes involved in hypoxia and cardiovascular diseases. In the absence of nitric oxide, it is not clear how HIF-1α and PHD are regulated and to what extent they contribute to the ensuing disorder.
Using the nitric oxide withdrawal/high salt diet model of hypertensive renal injury, this study tested the hypothesis that removal of the inhibition by nitric oxide on PHD predisposes to increased PHD but reduced HIF-1α expression, hypertension and renal injury.
In animals treated with N-nitro-L-arginine (L-NNA; 250 mg/l in drinking water for 14 days) and high salt diet (4% NaCl), there was hypertension (41±5%, P<0.05), proteinuria (three-fold, P<0.05), kidney (22±3%, P<0.05) and heart enlargement (24±3%, P<0.05), as well as increased renal osteopontin (21±3%, P<0.05) and collagen IV (24±4%, P<0.05) expression. Accompanying these effects were increased expression of PHD1 (24±4%, P<0.05) and PHD2 (36±4%, P<0.05) but reduced HIF-1α (35±6%, P < 0.05) expression. Dimethyloxallyl glycine (5mg/kg), a PHD inhibitor, paradoxically exacerbated hypertension (46±7%, P<0.05), proteinuria (two-fold, P <0.05), and increased osteopontin (15±2%, P<0.05) and HIF-1α (31±5%, P<0.05) expression with no change in PHD1/2 expression or kidney and heart enlargement.
These data suggest that the protective effect of physiological levels of nitric oxide may be by virtue of inhibition of PHD or increased HIF-1α expression, hence, the pathological changes produced following its withdrawal was accompanied by increased PHD or decreased HIF-1α expression. Exacerbation of hypertension and renal injury following PHD inhibition suggests a deleterious effect in the chronic setting and challenges the dogma that inhibition of PHD is useful in cardiovascular diseases.]]></abstract><cop>England</cop><pmid>23811999</pmid><doi>10.1097/HJH.0b013e32836356a0</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Blood Pressure Collagen Type IV - metabolism Female Gene Expression Regulation Hypertension - complications Hypertension - physiopathology Hypoxia - metabolism Hypoxia - pathology Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism Kidney - pathology Kidney Diseases - complications Kidney Diseases - metabolism Kidney Diseases - physiopathology Male Myocardium - pathology Nitric Oxide - physiology Nitric Oxide Synthase - antagonists & inhibitors Osteopontin - metabolism Oxidative Stress Protein Structure, Tertiary Proteinuria - complications Rats Rats, Sprague-Dawley Sodium Chloride, Dietary - adverse effects |
| title | Inhibition of prolyl hydroxylase domain-containing protein on hypertension/renal injury induced by high salt diet and nitric oxide withdrawal |
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