Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system
Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system. Male gender confers enhanced susceptibility to development of age-dependent kidney damage. In other models of progressive renal disease, development of injury is linked to declines in renal nitric oxide synthase (NOS)...
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description | Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system.
Male gender confers enhanced susceptibility to development of age-dependent kidney damage. In other models of progressive renal disease, development of injury is linked to declines in renal nitric oxide synthase (NOS) capacity.
We investigated the in vitro characteristics of the renal NOS system in young (3 to 5 months), middle-aged (11 to 13 months) and old (18 to 22 months) male and female Sprague-Dawley rats.
NOS activity (pmol [3H]-arginine converted to [3H]-citrulline/mg protein/minute) is reduced in the soluble fraction of renal cortex from old versus young males but not females. In contrast, NOS activity in the soluble fraction of cerebellum is not altered by age or gender. The abundance of endothelial NOS (eNOS) and neuronal (nNOS) is reduced in renal cortex of old versus young males but is unchanged in female cortex. In renal medulla, eNOS protein is reduced with age in both males and females. We found no difference in abundance of either eNOS or nNOS protein in the cortex of young male and female rats. The incidence and severity of glomerular damage increases markedly with age in the male and only slightly in the female.
These findings indicate that a relative reduction occurs in renal NOS in the male kidney with advancing age, whereas NOS protein and activity is maintained during aging in females. This, together with the marked age-dependent kidney damage seen in the male, suggests that the renal NO deficiency in the aging male rat may contribute to the age-dependent kidney damage. |
doi_str_mv | 10.1046/j.1523-1755.2003.00830.x |
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Male gender confers enhanced susceptibility to development of age-dependent kidney damage. In other models of progressive renal disease, development of injury is linked to declines in renal nitric oxide synthase (NOS) capacity.
We investigated the in vitro characteristics of the renal NOS system in young (3 to 5 months), middle-aged (11 to 13 months) and old (18 to 22 months) male and female Sprague-Dawley rats.
NOS activity (pmol [3H]-arginine converted to [3H]-citrulline/mg protein/minute) is reduced in the soluble fraction of renal cortex from old versus young males but not females. In contrast, NOS activity in the soluble fraction of cerebellum is not altered by age or gender. The abundance of endothelial NOS (eNOS) and neuronal (nNOS) is reduced in renal cortex of old versus young males but is unchanged in female cortex. In renal medulla, eNOS protein is reduced with age in both males and females. We found no difference in abundance of either eNOS or nNOS protein in the cortex of young male and female rats. The incidence and severity of glomerular damage increases markedly with age in the male and only slightly in the female.
These findings indicate that a relative reduction occurs in renal NOS in the male kidney with advancing age, whereas NOS protein and activity is maintained during aging in females. This, together with the marked age-dependent kidney damage seen in the male, suggests that the renal NO deficiency in the aging male rat may contribute to the age-dependent kidney damage.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1046/j.1523-1755.2003.00830.x</identifier><identifier>PMID: 12631083</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Aging - physiology ; Animals ; Biological and medical sciences ; endothelial nitric oxide synthase ; Female ; Glomerulonephritis ; glomerulosclerosis ; kidney cortex ; Kidney Cortex - metabolism ; Kidney Diseases - physiopathology ; kidney medulla ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; neuronal nitric oxide synthase ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - metabolism ; nitric oxide synthase activity ; Nitric Oxide Synthase Type I ; Nitric Oxide Synthase Type III ; Rats ; Rats, Sprague-Dawley ; Sex Characteristics</subject><ispartof>Kidney international, 2003-03, Vol.63 (3), p.1021-1026</ispartof><rights>2003 International Society of Nephrology</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 2003</rights><rights>2003 by the International Society of Nephrology 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c620t-c8e937987b1a31a2962cf54122cb983629e883e16998191574148aabeebc02543</citedby><cites>FETCH-LOGICAL-c620t-c8e937987b1a31a2962cf54122cb983629e883e16998191574148aabeebc02543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210107097?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15144137$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12631083$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Erdely, Aaron</creatorcontrib><creatorcontrib>Greenfeld, Ziv</creatorcontrib><creatorcontrib>Wagner, Laszlo</creatorcontrib><creatorcontrib>Baylis, Chris</creatorcontrib><title>Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system.
Male gender confers enhanced susceptibility to development of age-dependent kidney damage. In other models of progressive renal disease, development of injury is linked to declines in renal nitric oxide synthase (NOS) capacity.
We investigated the in vitro characteristics of the renal NOS system in young (3 to 5 months), middle-aged (11 to 13 months) and old (18 to 22 months) male and female Sprague-Dawley rats.
NOS activity (pmol [3H]-arginine converted to [3H]-citrulline/mg protein/minute) is reduced in the soluble fraction of renal cortex from old versus young males but not females. In contrast, NOS activity in the soluble fraction of cerebellum is not altered by age or gender. The abundance of endothelial NOS (eNOS) and neuronal (nNOS) is reduced in renal cortex of old versus young males but is unchanged in female cortex. In renal medulla, eNOS protein is reduced with age in both males and females. We found no difference in abundance of either eNOS or nNOS protein in the cortex of young male and female rats. The incidence and severity of glomerular damage increases markedly with age in the male and only slightly in the female.
These findings indicate that a relative reduction occurs in renal NOS in the male kidney with advancing age, whereas NOS protein and activity is maintained during aging in females. This, together with the marked age-dependent kidney damage seen in the male, suggests that the renal NO deficiency in the aging male rat may contribute to the age-dependent kidney damage.</description><subject>Aging - physiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>endothelial nitric oxide synthase</subject><subject>Female</subject><subject>Glomerulonephritis</subject><subject>glomerulosclerosis</subject><subject>kidney cortex</subject><subject>Kidney Cortex - metabolism</subject><subject>Kidney Diseases - physiopathology</subject><subject>kidney medulla</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>neuronal nitric oxide synthase</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>nitric oxide synthase activity</subject><subject>Nitric Oxide Synthase Type I</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sex Characteristics</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkVuL1DAYhoMo7rj6E5Qg6F27OfSQeCHosu4KCwrqdUjTrzOpbTIm7TLz702dYVa92auQvM93CA9CmJKckqK66HNaMp7RuixzRgjPCRGc5LtHaHUKHqNVei0zVnJxhp7F2JN0l5w8RWeUVZymkhX6-g12sx5wa0cfthsbR2wdnjaA9dq6Nf5pWwf7d_iq68BMEXuX8n4Oe6xdi52dgjXY72wLOO7jBONz9KTTQ4QXx_Mc_fh09f3yJrv9cv358sNtZipGpswIkLyWom6o5lQzWTHTlQVlzDRS8IpJEIIDraQUVNKyLmghtG4AGkNYWfBz9P7Qdzs3I7QG3BT0oLbBjjrslddW_Zs4u1Frf6dYLXklaGrw9tgg-F8zxEmNNhoYBu3Az1HVnEgu2DLp9X9g7-fg0ucUo4SSmsg6QeIAmeBjDNCdNqFELc5UrxY1alGjFmfqjzO1S6Wv_v7JfeFRUgLeHAEdjR66oJ2x8Z4raVFQvuzw8sA5Pc0BTkBRSJ5Gp_zjIYfk5c5CUNFYcAZaG5Jc1Xr78La_AfJdvk4</recordid><startdate>20030301</startdate><enddate>20030301</enddate><creator>Erdely, Aaron</creator><creator>Greenfeld, Ziv</creator><creator>Wagner, Laszlo</creator><creator>Baylis, Chris</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20030301</creationdate><title>Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system</title><author>Erdely, Aaron ; Greenfeld, Ziv ; Wagner, Laszlo ; Baylis, Chris</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c620t-c8e937987b1a31a2962cf54122cb983629e883e16998191574148aabeebc02543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Aging - physiology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>endothelial nitric oxide synthase</topic><topic>Female</topic><topic>Glomerulonephritis</topic><topic>glomerulosclerosis</topic><topic>kidney cortex</topic><topic>Kidney Cortex - metabolism</topic><topic>Kidney Diseases - physiopathology</topic><topic>kidney medulla</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>neuronal nitric oxide synthase</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>nitric oxide synthase activity</topic><topic>Nitric Oxide Synthase Type I</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sex Characteristics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Erdely, Aaron</creatorcontrib><creatorcontrib>Greenfeld, Ziv</creatorcontrib><creatorcontrib>Wagner, Laszlo</creatorcontrib><creatorcontrib>Baylis, Chris</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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 Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Erdely, Aaron</au><au>Greenfeld, Ziv</au><au>Wagner, Laszlo</au><au>Baylis, Chris</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2003-03-01</date><risdate>2003</risdate><volume>63</volume><issue>3</issue><spage>1021</spage><epage>1026</epage><pages>1021-1026</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system.
Male gender confers enhanced susceptibility to development of age-dependent kidney damage. In other models of progressive renal disease, development of injury is linked to declines in renal nitric oxide synthase (NOS) capacity.
We investigated the in vitro characteristics of the renal NOS system in young (3 to 5 months), middle-aged (11 to 13 months) and old (18 to 22 months) male and female Sprague-Dawley rats.
NOS activity (pmol [3H]-arginine converted to [3H]-citrulline/mg protein/minute) is reduced in the soluble fraction of renal cortex from old versus young males but not females. In contrast, NOS activity in the soluble fraction of cerebellum is not altered by age or gender. The abundance of endothelial NOS (eNOS) and neuronal (nNOS) is reduced in renal cortex of old versus young males but is unchanged in female cortex. In renal medulla, eNOS protein is reduced with age in both males and females. We found no difference in abundance of either eNOS or nNOS protein in the cortex of young male and female rats. The incidence and severity of glomerular damage increases markedly with age in the male and only slightly in the female.
These findings indicate that a relative reduction occurs in renal NOS in the male kidney with advancing age, whereas NOS protein and activity is maintained during aging in females. This, together with the marked age-dependent kidney damage seen in the male, suggests that the renal NO deficiency in the aging male rat may contribute to the age-dependent kidney damage.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>12631083</pmid><doi>10.1046/j.1523-1755.2003.00830.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aging - physiology Animals Biological and medical sciences endothelial nitric oxide synthase Female Glomerulonephritis glomerulosclerosis kidney cortex Kidney Cortex - metabolism Kidney Diseases - physiopathology kidney medulla Male Medical sciences Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure neuronal nitric oxide synthase Nitric Oxide - metabolism Nitric Oxide Synthase - metabolism nitric oxide synthase activity Nitric Oxide Synthase Type I Nitric Oxide Synthase Type III Rats Rats, Sprague-Dawley Sex Characteristics |
title | Sexual dimorphism in the aging kidney: Effects on injury and nitric oxide system |
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