Enhanced sensitivity to acute angiotensin II is testosterone dependent in adult male growth-restricted offspring
Placental insufficiency results in intrauterine growth restriction (IUGR) and hypertension in adult male growth-restricted rats. Although renal ANG II and plasma renin activity do not differ between growth-restricted and control rats, blockade of the renin-angiotensin system (RAS) abolishes hyperten...
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| Veröffentlicht in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2010-05, Vol.298 (5), p.R1421-R1427 |
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| container_title | American journal of physiology. Regulatory, integrative and comparative physiology |
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| creator | Ojeda, Norma B Royals, Thomas P Black, Joshua T Dasinger, John Henry Johnson, Jeremy M Alexander, Barbara T |
| description | Placental insufficiency results in intrauterine growth restriction (IUGR) and hypertension in adult male growth-restricted rats. Although renal ANG II and plasma renin activity do not differ between growth-restricted and control rats, blockade of the renin-angiotensin system (RAS) abolishes hypertension in growth-restricted rats, suggesting that the RAS contributes to IUGR-induced hypertension. Moreover, castration abolishes hypertension in growth-restricted rats, indicating an important role for testosterone. Therefore, we hypothesized that enhanced responsiveness to ANG II contributes to hypertension in this model of IUGR and that androgens may play a pivotal role in this enhanced response. Physiological parameters were determined at 16 wk of age in male rats pretreated with enalapril (40 mg.kg(-1).day(-1)) for 1 wk. Baseline blood pressures were similar between growth-restricted (112 +/- 3 mmHg) and control (110 +/- 2 mmHg) rats; however, an enhanced pressor response to acute ANG II (100 ng.kg(-1).min(-1) for 30 min) was observed in growth-restricted (160 +/- 2 mmHg) vs. control (136 +/- 2 mmHg; P < 0.05) rats. Castration abolished the enhanced pressor response to acute ANG II in growth-restricted (130 +/- 2 mmHg) rats with no significant effect on blood pressure in controls (130 +/- 2 mmHg). Blood pressure was increased to a similar extent above baseline in response to acute phenylephrine (100 microg/min) in control (184 +/- 5 mmHg) and growth-restricted (184 +/- 8 mmHg) rats, suggesting the enhanced pressor response in growth-restricted rats is ANG II specific. Thus, these results suggest that growth-restricted rats exhibit an enhanced responsiveness to ANG II that is testosterone dependent and indicate that the RAS may serve as an underlying mechanism in mediating hypertension programmed in response to IUGR. |
| doi_str_mv | 10.1152/ajpregu.00096.2010 |
| format | Article |
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Although renal ANG II and plasma renin activity do not differ between growth-restricted and control rats, blockade of the renin-angiotensin system (RAS) abolishes hypertension in growth-restricted rats, suggesting that the RAS contributes to IUGR-induced hypertension. Moreover, castration abolishes hypertension in growth-restricted rats, indicating an important role for testosterone. Therefore, we hypothesized that enhanced responsiveness to ANG II contributes to hypertension in this model of IUGR and that androgens may play a pivotal role in this enhanced response. Physiological parameters were determined at 16 wk of age in male rats pretreated with enalapril (40 mg.kg(-1).day(-1)) for 1 wk. Baseline blood pressures were similar between growth-restricted (112 +/- 3 mmHg) and control (110 +/- 2 mmHg) rats; however, an enhanced pressor response to acute ANG II (100 ng.kg(-1).min(-1) for 30 min) was observed in growth-restricted (160 +/- 2 mmHg) vs. control (136 +/- 2 mmHg; P < 0.05) rats. Castration abolished the enhanced pressor response to acute ANG II in growth-restricted (130 +/- 2 mmHg) rats with no significant effect on blood pressure in controls (130 +/- 2 mmHg). Blood pressure was increased to a similar extent above baseline in response to acute phenylephrine (100 microg/min) in control (184 +/- 5 mmHg) and growth-restricted (184 +/- 8 mmHg) rats, suggesting the enhanced pressor response in growth-restricted rats is ANG II specific. Thus, these results suggest that growth-restricted rats exhibit an enhanced responsiveness to ANG II that is testosterone dependent and indicate that the RAS may serve as an underlying mechanism in mediating hypertension programmed in response to IUGR.</description><identifier>ISSN: 0363-6119</identifier><identifier>ISSN: 1522-1490</identifier><identifier>EISSN: 1522-1490</identifier><identifier>DOI: 10.1152/ajpregu.00096.2010</identifier><identifier>PMID: 20219873</identifier><identifier>CODEN: AJPRDO</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Age Factors ; Angiotensin II - pharmacology ; Animals ; Birth Weight - physiology ; Blood pressure ; Blood Pressure - physiology ; Body Weight - physiology ; Drinking - physiology ; Female ; Fetal Growth Retardation - physiopathology ; Hypertension ; Hypertension, Renal - etiology ; Hypertension, Renal - physiopathology ; Kidney - anatomy & histology ; Kidney - physiology ; Male ; Orchiectomy ; Organ Size - physiology ; Phenylephrine - pharmacology ; Physiology ; Plasma ; Pregnancy ; Prenatal Exposure Delayed Effects - physiopathology ; Proteins ; Rats ; Rats, Sprague-Dawley ; Renin-Angiotensin System - drug effects ; Renin-Angiotensin System - physiology ; Rodents ; Sex Factors ; Testosterone ; Testosterone - blood ; Testosterone - physiology ; Vasoconstrictor Agents - pharmacology</subject><ispartof>American journal of physiology. Regulatory, integrative and comparative physiology, 2010-05, Vol.298 (5), p.R1421-R1427</ispartof><rights>Copyright American Physiological Society May 2010</rights><rights>Copyright © 2010 the American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-49c3cc706f48c8dd6645205e59867dd2e2c59a4454bdde74d0835e1f68e4afc43</citedby><cites>FETCH-LOGICAL-c494t-49c3cc706f48c8dd6645205e59867dd2e2c59a4454bdde74d0835e1f68e4afc43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20219873$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ojeda, Norma B</creatorcontrib><creatorcontrib>Royals, Thomas P</creatorcontrib><creatorcontrib>Black, Joshua T</creatorcontrib><creatorcontrib>Dasinger, John Henry</creatorcontrib><creatorcontrib>Johnson, Jeremy M</creatorcontrib><creatorcontrib>Alexander, Barbara T</creatorcontrib><title>Enhanced sensitivity to acute angiotensin II is testosterone dependent in adult male growth-restricted offspring</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><description>Placental insufficiency results in intrauterine growth restriction (IUGR) and hypertension in adult male growth-restricted rats. Although renal ANG II and plasma renin activity do not differ between growth-restricted and control rats, blockade of the renin-angiotensin system (RAS) abolishes hypertension in growth-restricted rats, suggesting that the RAS contributes to IUGR-induced hypertension. Moreover, castration abolishes hypertension in growth-restricted rats, indicating an important role for testosterone. Therefore, we hypothesized that enhanced responsiveness to ANG II contributes to hypertension in this model of IUGR and that androgens may play a pivotal role in this enhanced response. Physiological parameters were determined at 16 wk of age in male rats pretreated with enalapril (40 mg.kg(-1).day(-1)) for 1 wk. Baseline blood pressures were similar between growth-restricted (112 +/- 3 mmHg) and control (110 +/- 2 mmHg) rats; however, an enhanced pressor response to acute ANG II (100 ng.kg(-1).min(-1) for 30 min) was observed in growth-restricted (160 +/- 2 mmHg) vs. control (136 +/- 2 mmHg; P < 0.05) rats. Castration abolished the enhanced pressor response to acute ANG II in growth-restricted (130 +/- 2 mmHg) rats with no significant effect on blood pressure in controls (130 +/- 2 mmHg). Blood pressure was increased to a similar extent above baseline in response to acute phenylephrine (100 microg/min) in control (184 +/- 5 mmHg) and growth-restricted (184 +/- 8 mmHg) rats, suggesting the enhanced pressor response in growth-restricted rats is ANG II specific. Thus, these results suggest that growth-restricted rats exhibit an enhanced responsiveness to ANG II that is testosterone dependent and indicate that the RAS may serve as an underlying mechanism in mediating hypertension programmed in response to IUGR.</description><subject>Age Factors</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Birth Weight - physiology</subject><subject>Blood pressure</subject><subject>Blood Pressure - physiology</subject><subject>Body Weight - physiology</subject><subject>Drinking - physiology</subject><subject>Female</subject><subject>Fetal Growth Retardation - physiopathology</subject><subject>Hypertension</subject><subject>Hypertension, Renal - etiology</subject><subject>Hypertension, Renal - physiopathology</subject><subject>Kidney - anatomy & histology</subject><subject>Kidney - physiology</subject><subject>Male</subject><subject>Orchiectomy</subject><subject>Organ Size - physiology</subject><subject>Phenylephrine - pharmacology</subject><subject>Physiology</subject><subject>Plasma</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects - physiopathology</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Renin-Angiotensin System - physiology</subject><subject>Rodents</subject><subject>Sex Factors</subject><subject>Testosterone</subject><subject>Testosterone - blood</subject><subject>Testosterone - physiology</subject><subject>Vasoconstrictor Agents - pharmacology</subject><issn>0363-6119</issn><issn>1522-1490</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1v1DAYhC0EokvhD3BAFhdO2foziS9IqCqwUqVe2rPl2m-yXmXtYDtF_fc4dKmAkw_zvOMZDULvKdlSKtmFOcwJxmVLCFHtlhFKXqBNFVhDhSIv0YbwljctpeoMvcn5UDnBBX-NzhhhVPUd36D5KuxNsOBwhpB98Q--POISsbFLAWzC6GNZlYB3O-wzLpBLzAVSDIAdzBAchIKrbtwyFXw0E-AxxZ9l36TKJm9LdY_DkOfkw_gWvRrMlOHd6T1Hd1-vbi-_N9c333aXX64bK5QojVCWW9uRdhC97Z1rWyEZkSBV33bOMWBWKiOEFPfOQScc6bkEOrQ9CDNYwc_R5yffebk_grM1ZDKTrhmOJj3qaLz-Vwl-r8f4oFn9QNLV4NPJIMUfS22ijz5bmCYTIC5Zd6JXUgnOKvnxP_IQlxRqO81Y3YazfoXYE2RTzDnB8ByFEr3OqU9z6t9z6nXOevTh7xLPJ3_2478AxnWghw</recordid><startdate>20100501</startdate><enddate>20100501</enddate><creator>Ojeda, Norma B</creator><creator>Royals, Thomas P</creator><creator>Black, Joshua T</creator><creator>Dasinger, John Henry</creator><creator>Johnson, Jeremy M</creator><creator>Alexander, Barbara T</creator><general>American Physiological Society</general><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>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100501</creationdate><title>Enhanced sensitivity to acute angiotensin II is testosterone dependent in adult male growth-restricted offspring</title><author>Ojeda, Norma B ; Royals, Thomas P ; Black, Joshua T ; Dasinger, John Henry ; Johnson, Jeremy M ; Alexander, Barbara T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-49c3cc706f48c8dd6645205e59867dd2e2c59a4454bdde74d0835e1f68e4afc43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Age Factors</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Birth Weight - physiology</topic><topic>Blood pressure</topic><topic>Blood Pressure - physiology</topic><topic>Body Weight - physiology</topic><topic>Drinking - physiology</topic><topic>Female</topic><topic>Fetal Growth Retardation - physiopathology</topic><topic>Hypertension</topic><topic>Hypertension, Renal - etiology</topic><topic>Hypertension, Renal - physiopathology</topic><topic>Kidney - anatomy & histology</topic><topic>Kidney - physiology</topic><topic>Male</topic><topic>Orchiectomy</topic><topic>Organ Size - physiology</topic><topic>Phenylephrine - pharmacology</topic><topic>Physiology</topic><topic>Plasma</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects - physiopathology</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Renin-Angiotensin System - physiology</topic><topic>Rodents</topic><topic>Sex Factors</topic><topic>Testosterone</topic><topic>Testosterone - blood</topic><topic>Testosterone - physiology</topic><topic>Vasoconstrictor Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ojeda, Norma B</creatorcontrib><creatorcontrib>Royals, Thomas P</creatorcontrib><creatorcontrib>Black, Joshua T</creatorcontrib><creatorcontrib>Dasinger, John Henry</creatorcontrib><creatorcontrib>Johnson, Jeremy M</creatorcontrib><creatorcontrib>Alexander, Barbara T</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ojeda, Norma B</au><au>Royals, Thomas P</au><au>Black, Joshua T</au><au>Dasinger, John Henry</au><au>Johnson, Jeremy M</au><au>Alexander, Barbara T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced sensitivity to acute angiotensin II is testosterone dependent in adult male growth-restricted offspring</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><date>2010-05-01</date><risdate>2010</risdate><volume>298</volume><issue>5</issue><spage>R1421</spage><epage>R1427</epage><pages>R1421-R1427</pages><issn>0363-6119</issn><issn>1522-1490</issn><eissn>1522-1490</eissn><coden>AJPRDO</coden><abstract>Placental insufficiency results in intrauterine growth restriction (IUGR) and hypertension in adult male growth-restricted rats. Although renal ANG II and plasma renin activity do not differ between growth-restricted and control rats, blockade of the renin-angiotensin system (RAS) abolishes hypertension in growth-restricted rats, suggesting that the RAS contributes to IUGR-induced hypertension. Moreover, castration abolishes hypertension in growth-restricted rats, indicating an important role for testosterone. Therefore, we hypothesized that enhanced responsiveness to ANG II contributes to hypertension in this model of IUGR and that androgens may play a pivotal role in this enhanced response. Physiological parameters were determined at 16 wk of age in male rats pretreated with enalapril (40 mg.kg(-1).day(-1)) for 1 wk. Baseline blood pressures were similar between growth-restricted (112 +/- 3 mmHg) and control (110 +/- 2 mmHg) rats; however, an enhanced pressor response to acute ANG II (100 ng.kg(-1).min(-1) for 30 min) was observed in growth-restricted (160 +/- 2 mmHg) vs. control (136 +/- 2 mmHg; P < 0.05) rats. Castration abolished the enhanced pressor response to acute ANG II in growth-restricted (130 +/- 2 mmHg) rats with no significant effect on blood pressure in controls (130 +/- 2 mmHg). Blood pressure was increased to a similar extent above baseline in response to acute phenylephrine (100 microg/min) in control (184 +/- 5 mmHg) and growth-restricted (184 +/- 8 mmHg) rats, suggesting the enhanced pressor response in growth-restricted rats is ANG II specific. Thus, these results suggest that growth-restricted rats exhibit an enhanced responsiveness to ANG II that is testosterone dependent and indicate that the RAS may serve as an underlying mechanism in mediating hypertension programmed in response to IUGR.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>20219873</pmid><doi>10.1152/ajpregu.00096.2010</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Age Factors Angiotensin II - pharmacology Animals Birth Weight - physiology Blood pressure Blood Pressure - physiology Body Weight - physiology Drinking - physiology Female Fetal Growth Retardation - physiopathology Hypertension Hypertension, Renal - etiology Hypertension, Renal - physiopathology Kidney - anatomy & histology Kidney - physiology Male Orchiectomy Organ Size - physiology Phenylephrine - pharmacology Physiology Plasma Pregnancy Prenatal Exposure Delayed Effects - physiopathology Proteins Rats Rats, Sprague-Dawley Renin-Angiotensin System - drug effects Renin-Angiotensin System - physiology Rodents Sex Factors Testosterone Testosterone - blood Testosterone - physiology Vasoconstrictor Agents - pharmacology |
| title | Enhanced sensitivity to acute angiotensin II is testosterone dependent in adult male growth-restricted offspring |
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