Maternal Glucocorticoid Treatment Programs Alterations in the Renin-Angiotensin System of the Ovine Fetal Kidney
Ovine fetuses exposed to high concentrations of synthetic (dexamethasone, D) or naturally occurring glucocorticoids (cortisol, F) in utero during early gestation develop high blood pressure in adulthood. To investigate potential mechanisms involved, we examined the role of the renal renin-angiotensi...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2002-11, Vol.143 (11), p.4455-4463 |
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| creator | Moritz, K. M Johnson, K Douglas-Denton, R Wintour, E. M Dodic, M |
| description | Ovine fetuses exposed to high concentrations of synthetic (dexamethasone, D) or naturally occurring glucocorticoids (cortisol, F) in utero during early gestation develop high blood pressure in adulthood. To investigate potential mechanisms involved, we examined the role of the renal renin-angiotensin system (RAS). Ewes were infused with isotonic saline (S, n = 11), D (n = 12, 0.48 mg/h), or F (n = 5, 5 mg/h) for 48 h between d 26 and 28 of gestation (term = 150 d). Ewes carrying twins (S, n = 5; D, n = 6; F, n = 5) were killed at 130 d of gestation. The mRNA levels for angiotensinogen, the AT1 receptor and AT2 receptor, were increased in the fetal kidneys after D treatment. Prenatal infusions of F produced similar effects on the AT1 receptor. Single fetuses (S, n = 6; D, n = 6) were cannulated and infused with angiotensin II for 3 d beginning at 127 d of gestation. Basal blood pressure was similar in both groups and increased similarly with angiotensin II infusion. However, increases in urine flow and glomerular filtration rate were significantly reduced and kidney weights increased in the D-treated group. These results indicate that treatment with D very early in gestation causes significant alterations in the RAS in the fetal kidney 100 d later with functional consequences. Changes in the RAS in the developing kidney may be an important mechanism in the development of adult disease. |
| doi_str_mv | 10.1210/en.2002-220534 |
| format | Article |
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M ; Johnson, K ; Douglas-Denton, R ; Wintour, E. M ; Dodic, M</creator><creatorcontrib>Moritz, K. M ; Johnson, K ; Douglas-Denton, R ; Wintour, E. M ; Dodic, M</creatorcontrib><description>Ovine fetuses exposed to high concentrations of synthetic (dexamethasone, D) or naturally occurring glucocorticoids (cortisol, F) in utero during early gestation develop high blood pressure in adulthood. To investigate potential mechanisms involved, we examined the role of the renal renin-angiotensin system (RAS). Ewes were infused with isotonic saline (S, n = 11), D (n = 12, 0.48 mg/h), or F (n = 5, 5 mg/h) for 48 h between d 26 and 28 of gestation (term = 150 d). Ewes carrying twins (S, n = 5; D, n = 6; F, n = 5) were killed at 130 d of gestation. The mRNA levels for angiotensinogen, the AT1 receptor and AT2 receptor, were increased in the fetal kidneys after D treatment. Prenatal infusions of F produced similar effects on the AT1 receptor. Single fetuses (S, n = 6; D, n = 6) were cannulated and infused with angiotensin II for 3 d beginning at 127 d of gestation. Basal blood pressure was similar in both groups and increased similarly with angiotensin II infusion. However, increases in urine flow and glomerular filtration rate were significantly reduced and kidney weights increased in the D-treated group. These results indicate that treatment with D very early in gestation causes significant alterations in the RAS in the fetal kidney 100 d later with functional consequences. Changes in the RAS in the developing kidney may be an important mechanism in the development of adult disease.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2002-220534</identifier><identifier>PMID: 12399443</identifier><language>eng</language><publisher>United States: Endocrine Society</publisher><subject>Angiotensin ; Angiotensin II ; Angiotensin II - administration & dosage ; Angiotensinogen ; Angiotensinogen - genetics ; Animals ; Blood pressure ; Blood Pressure - drug effects ; Blotting, Western ; Dexamethasone ; Dexamethasone - administration & dosage ; Dexamethasone - adverse effects ; Diuresis - drug effects ; Endocrine system ; Female ; Fetuses ; Gestation ; Gestational Age ; Glomerular filtration rate ; Glomerular Filtration Rate - drug effects ; Glucocorticoids ; Glucocorticoids - administration & dosage ; Glucocorticoids - adverse effects ; Hydrocortisone - administration & dosage ; Hydrocortisone - adverse effects ; Hypertension ; Hypertension - chemically induced ; Immunohistochemistry ; Kidney - embryology ; Kidney - physiology ; Kidneys ; Maternal-Fetal Exchange ; mRNA ; Nucleic Acid Hybridization ; Organ Size - drug effects ; Polymerase Chain Reaction ; Pregnancy ; Prenatal Exposure Delayed Effects ; Receptor, Angiotensin, Type 1 ; Receptor, Angiotensin, Type 2 ; Receptors ; Receptors, Angiotensin - genetics ; Renin ; Renin-Angiotensin System - drug effects ; RNA, Messenger - analysis ; Sheep</subject><ispartof>Endocrinology (Philadelphia), 2002-11, Vol.143 (11), p.4455-4463</ispartof><rights>Copyright © 2002 by The Endocrine Society 2002</rights><rights>Copyright © 2002 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-6e3f325f20d9658f0d2392c41911e75cf4013de0d6b0b28fbbd56efb5da612483</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12399443$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moritz, K. M</creatorcontrib><creatorcontrib>Johnson, K</creatorcontrib><creatorcontrib>Douglas-Denton, R</creatorcontrib><creatorcontrib>Wintour, E. M</creatorcontrib><creatorcontrib>Dodic, M</creatorcontrib><title>Maternal Glucocorticoid Treatment Programs Alterations in the Renin-Angiotensin System of the Ovine Fetal Kidney</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Ovine fetuses exposed to high concentrations of synthetic (dexamethasone, D) or naturally occurring glucocorticoids (cortisol, F) in utero during early gestation develop high blood pressure in adulthood. To investigate potential mechanisms involved, we examined the role of the renal renin-angiotensin system (RAS). Ewes were infused with isotonic saline (S, n = 11), D (n = 12, 0.48 mg/h), or F (n = 5, 5 mg/h) for 48 h between d 26 and 28 of gestation (term = 150 d). Ewes carrying twins (S, n = 5; D, n = 6; F, n = 5) were killed at 130 d of gestation. The mRNA levels for angiotensinogen, the AT1 receptor and AT2 receptor, were increased in the fetal kidneys after D treatment. Prenatal infusions of F produced similar effects on the AT1 receptor. Single fetuses (S, n = 6; D, n = 6) were cannulated and infused with angiotensin II for 3 d beginning at 127 d of gestation. Basal blood pressure was similar in both groups and increased similarly with angiotensin II infusion. However, increases in urine flow and glomerular filtration rate were significantly reduced and kidney weights increased in the D-treated group. These results indicate that treatment with D very early in gestation causes significant alterations in the RAS in the fetal kidney 100 d later with functional consequences. Changes in the RAS in the developing kidney may be an important mechanism in the development of adult disease.</description><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - administration & dosage</subject><subject>Angiotensinogen</subject><subject>Angiotensinogen - genetics</subject><subject>Animals</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Blotting, Western</subject><subject>Dexamethasone</subject><subject>Dexamethasone - administration & dosage</subject><subject>Dexamethasone - adverse effects</subject><subject>Diuresis - drug effects</subject><subject>Endocrine system</subject><subject>Female</subject><subject>Fetuses</subject><subject>Gestation</subject><subject>Gestational Age</subject><subject>Glomerular filtration rate</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Glucocorticoids</subject><subject>Glucocorticoids - administration & dosage</subject><subject>Glucocorticoids - adverse effects</subject><subject>Hydrocortisone - administration & dosage</subject><subject>Hydrocortisone - adverse effects</subject><subject>Hypertension</subject><subject>Hypertension - chemically induced</subject><subject>Immunohistochemistry</subject><subject>Kidney - embryology</subject><subject>Kidney - physiology</subject><subject>Kidneys</subject><subject>Maternal-Fetal Exchange</subject><subject>mRNA</subject><subject>Nucleic Acid Hybridization</subject><subject>Organ Size - drug effects</subject><subject>Polymerase Chain Reaction</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Receptor, Angiotensin, Type 1</subject><subject>Receptor, Angiotensin, Type 2</subject><subject>Receptors</subject><subject>Receptors, Angiotensin - genetics</subject><subject>Renin</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>RNA, Messenger - analysis</subject><subject>Sheep</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kDtPwzAYRS0EgvJYGZElJoYUv5I0Y1XRgigC8ZijJP4Mrho72A5S_z0uqWBi8uv4-vogdE7JmDJKrsGMGSEsYYykXOyhES1EmuQ0J_toRAjlSc5YfoSOvV_FpRCCH6IjynhRxOkIdQ9VAGeqNV6s-8Y21gXdWC3xq4MqtGACfnL23VWtx9N1RKugrfFYGxw-AD-D0SaZmndtAxgfd182PkCLrfo5f_zSBvAcQnzgXksDm1N0oKq1h7PdeILe5jevs9tk-bi4m02XSROrhSQDrjhLFSOyyNKJIjJWZo2gBaWQp40S8W8SiMxqUrOJqmuZZqDqVFYZZWLCT9DlkNs5-9mDD-XK9tuP-pJTHmUxkWWRGg9U46z3DlTZOd1WblNSUm4Fl2DKreByEBwvXOxi-7oF-YfvjEbgagBs3_0XlvyGpQMLRtrGRVWdA-__mv5T4hvEUZSd</recordid><startdate>200211</startdate><enddate>200211</enddate><creator>Moritz, K. M</creator><creator>Johnson, K</creator><creator>Douglas-Denton, R</creator><creator>Wintour, E. M</creator><creator>Dodic, M</creator><general>Endocrine Society</general><general>Oxford University Press</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope></search><sort><creationdate>200211</creationdate><title>Maternal Glucocorticoid Treatment Programs Alterations in the Renin-Angiotensin System of the Ovine Fetal Kidney</title><author>Moritz, K. M ; Johnson, K ; Douglas-Denton, R ; Wintour, E. M ; Dodic, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-6e3f325f20d9658f0d2392c41911e75cf4013de0d6b0b28fbbd56efb5da612483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - administration & dosage</topic><topic>Angiotensinogen</topic><topic>Angiotensinogen - genetics</topic><topic>Animals</topic><topic>Blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>Blotting, Western</topic><topic>Dexamethasone</topic><topic>Dexamethasone - administration & dosage</topic><topic>Dexamethasone - adverse effects</topic><topic>Diuresis - drug effects</topic><topic>Endocrine system</topic><topic>Female</topic><topic>Fetuses</topic><topic>Gestation</topic><topic>Gestational Age</topic><topic>Glomerular filtration rate</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Glucocorticoids</topic><topic>Glucocorticoids - administration & dosage</topic><topic>Glucocorticoids - adverse effects</topic><topic>Hydrocortisone - administration & dosage</topic><topic>Hydrocortisone - adverse effects</topic><topic>Hypertension</topic><topic>Hypertension - chemically induced</topic><topic>Immunohistochemistry</topic><topic>Kidney - embryology</topic><topic>Kidney - physiology</topic><topic>Kidneys</topic><topic>Maternal-Fetal Exchange</topic><topic>mRNA</topic><topic>Nucleic Acid Hybridization</topic><topic>Organ Size - drug effects</topic><topic>Polymerase Chain Reaction</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects</topic><topic>Receptor, Angiotensin, Type 1</topic><topic>Receptor, Angiotensin, Type 2</topic><topic>Receptors</topic><topic>Receptors, Angiotensin - genetics</topic><topic>Renin</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>RNA, Messenger - analysis</topic><topic>Sheep</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moritz, K. 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M</au><au>Johnson, K</au><au>Douglas-Denton, R</au><au>Wintour, E. M</au><au>Dodic, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Maternal Glucocorticoid Treatment Programs Alterations in the Renin-Angiotensin System of the Ovine Fetal Kidney</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2002-11</date><risdate>2002</risdate><volume>143</volume><issue>11</issue><spage>4455</spage><epage>4463</epage><pages>4455-4463</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><abstract>Ovine fetuses exposed to high concentrations of synthetic (dexamethasone, D) or naturally occurring glucocorticoids (cortisol, F) in utero during early gestation develop high blood pressure in adulthood. To investigate potential mechanisms involved, we examined the role of the renal renin-angiotensin system (RAS). Ewes were infused with isotonic saline (S, n = 11), D (n = 12, 0.48 mg/h), or F (n = 5, 5 mg/h) for 48 h between d 26 and 28 of gestation (term = 150 d). Ewes carrying twins (S, n = 5; D, n = 6; F, n = 5) were killed at 130 d of gestation. The mRNA levels for angiotensinogen, the AT1 receptor and AT2 receptor, were increased in the fetal kidneys after D treatment. Prenatal infusions of F produced similar effects on the AT1 receptor. Single fetuses (S, n = 6; D, n = 6) were cannulated and infused with angiotensin II for 3 d beginning at 127 d of gestation. Basal blood pressure was similar in both groups and increased similarly with angiotensin II infusion. However, increases in urine flow and glomerular filtration rate were significantly reduced and kidney weights increased in the D-treated group. These results indicate that treatment with D very early in gestation causes significant alterations in the RAS in the fetal kidney 100 d later with functional consequences. Changes in the RAS in the developing kidney may be an important mechanism in the development of adult disease.</abstract><cop>United States</cop><pub>Endocrine Society</pub><pmid>12399443</pmid><doi>10.1210/en.2002-220534</doi><tpages>9</tpages></addata></record> |
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| subjects | Angiotensin Angiotensin II Angiotensin II - administration & dosage Angiotensinogen Angiotensinogen - genetics Animals Blood pressure Blood Pressure - drug effects Blotting, Western Dexamethasone Dexamethasone - administration & dosage Dexamethasone - adverse effects Diuresis - drug effects Endocrine system Female Fetuses Gestation Gestational Age Glomerular filtration rate Glomerular Filtration Rate - drug effects Glucocorticoids Glucocorticoids - administration & dosage Glucocorticoids - adverse effects Hydrocortisone - administration & dosage Hydrocortisone - adverse effects Hypertension Hypertension - chemically induced Immunohistochemistry Kidney - embryology Kidney - physiology Kidneys Maternal-Fetal Exchange mRNA Nucleic Acid Hybridization Organ Size - drug effects Polymerase Chain Reaction Pregnancy Prenatal Exposure Delayed Effects Receptor, Angiotensin, Type 1 Receptor, Angiotensin, Type 2 Receptors Receptors, Angiotensin - genetics Renin Renin-Angiotensin System - drug effects RNA, Messenger - analysis Sheep |
| title | Maternal Glucocorticoid Treatment Programs Alterations in the Renin-Angiotensin System of the Ovine Fetal Kidney |
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