Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure
Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. The mechanisms underlying this programmed elevation of blood pressure have not been established. We hypothesised that prenatal glucocorticoid exposure may lead to vascular dys...
Gespeichert in:
| Veröffentlicht in: | Journal of endocrinology 2006-03, Vol.188 (3), p.435-442 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 442 |
|---|---|
| container_issue | 3 |
| container_start_page | 435 |
| container_title | Journal of endocrinology |
| container_volume | 188 |
| creator | Hadoke, P W F Lindsay, R S Seckl, J R Walker, B R Kenyon, C J |
| description | Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. The mechanisms underlying this programmed elevation of blood pressure have not been established. We hypothesised that prenatal glucocorticoid exposure may lead to vascular dysfunction in adulthood. Pregnant rats received dexamethasone (Dex) (100 μg/kg, s.c.) or vehicle (control) daily throughout pregnancy. Blood pressure was elevated (students t-test, unpaired; P < 0.05) in adult female offspring (aged 12–16 weeks) of Dex-treated mothers (148.0 ± 3.6 mmHg, n=10) compared with the control group (138.0 ± 2.5 mmHg, n=8). Vascular responsiveness in aortae and mesenteric arteries was differentially affected by prenatal Dex: aortae were less responsive to angiotensin II, whereas mesenteric arteries were more responsive to norepinephrine, vasopressin and potassium (mesenteric arteries respond poorly to angiotensin II in vitro). Acetylcholine-mediated, endothelium-dependent relaxation was similar in both groups. Prenatal exposure to Dex had no effect on blood pressure or aldosterone response to acute (15 min, i.v.) infusion of angiotensin II (75 ng/kg per min). In contrast, chronic (2-week, s.c.) infusion of angiotensin II (100 ng/kg per min) produced a greater elevation (P < 0.05) of blood pressure in Dex-treated rats (150.0 ± 3.6 mmHg) than in controls (135.3 ± 5.4 mmHg), and aldosterone levels were higher in Dex-treated animals. There was no angiotensin II-induced medial hypertrophy/hyperplasia in mesenteric arteries from Dex-treated rats. These results indicate that vascular function is altered in a region-specific manner in rats with glucocorticoid-programmed hypertension. Despite a striking increase in mesenteric artery contraction in Dex-treated rats, in vivo studies suggest that abnormalities of the renin-angiotensin-aldosterone system, rather than enhanced vascular contractility, may be responsible for the elevation of blood pressure in these animals. |
| doi_str_mv | 10.1677/joe.1.06506 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67731737</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67731737</sourcerecordid><originalsourceid>FETCH-LOGICAL-b439t-ec13ef4ecd3c8ed878b6773d2e8acf2ddd02801854b39d74862d450a259eb2083</originalsourceid><addsrcrecordid>eNp9kMFLHDEUh0NpqavtqXfJpb3IbJPMZJI5ilQrCF7qOWSSN7uRzGRNMur-92bdBUGop8eD7_3eex9CPyhZ0laI3_cBlnRJWk7aT2hBG9FVrST8M1oQwlhFRMeP0HFK94RQTkX9FR3RljMmWLNA-dxniGDxo05m9jpiE6YctcnOu7zFbsLazj7jAUbtAUedE35yeY3X2w3EDFNyYcKbGFZRj2MJ6relg0ln7fHKzyaYELMzwVkMz5uQ5gjf0JdB-wTfD_UE3V3--Xfxt7q5vbq-OL-p-qbucgWG1jA0YGxtJFgpZF_-rS0Dqc3ArLWESUIlb_q6s6KRLbMNJ5rxDnpGZH2Cfu1zy3kPM6SsRpcMeK8nCHNSu7QiRBTwbA-aGFKKMKhNdKOOW0WJ2klWRbKi6lVyoU8PsXNfPn5jD1YL8PMAFKnaD1FPxqU3TvCu6drdWrbn1m61fnIRVO9CMg6m7AZn9H-20_3QO_aji18A0vup0w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67731737</pqid></control><display><type>article</type><title>Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure</title><source>MEDLINE</source><source>EZB Electronic Journals Library</source><creator>Hadoke, P W F ; Lindsay, R S ; Seckl, J R ; Walker, B R ; Kenyon, C J</creator><creatorcontrib>Hadoke, P W F ; Lindsay, R S ; Seckl, J R ; Walker, B R ; Kenyon, C J</creatorcontrib><description>Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. The mechanisms underlying this programmed elevation of blood pressure have not been established. We hypothesised that prenatal glucocorticoid exposure may lead to vascular dysfunction in adulthood. Pregnant rats received dexamethasone (Dex) (100 μg/kg, s.c.) or vehicle (control) daily throughout pregnancy. Blood pressure was elevated (students t-test, unpaired; P < 0.05) in adult female offspring (aged 12–16 weeks) of Dex-treated mothers (148.0 ± 3.6 mmHg, n=10) compared with the control group (138.0 ± 2.5 mmHg, n=8). Vascular responsiveness in aortae and mesenteric arteries was differentially affected by prenatal Dex: aortae were less responsive to angiotensin II, whereas mesenteric arteries were more responsive to norepinephrine, vasopressin and potassium (mesenteric arteries respond poorly to angiotensin II in vitro). Acetylcholine-mediated, endothelium-dependent relaxation was similar in both groups. Prenatal exposure to Dex had no effect on blood pressure or aldosterone response to acute (15 min, i.v.) infusion of angiotensin II (75 ng/kg per min). In contrast, chronic (2-week, s.c.) infusion of angiotensin II (100 ng/kg per min) produced a greater elevation (P < 0.05) of blood pressure in Dex-treated rats (150.0 ± 3.6 mmHg) than in controls (135.3 ± 5.4 mmHg), and aldosterone levels were higher in Dex-treated animals. There was no angiotensin II-induced medial hypertrophy/hyperplasia in mesenteric arteries from Dex-treated rats. These results indicate that vascular function is altered in a region-specific manner in rats with glucocorticoid-programmed hypertension. Despite a striking increase in mesenteric artery contraction in Dex-treated rats, in vivo studies suggest that abnormalities of the renin-angiotensin-aldosterone system, rather than enhanced vascular contractility, may be responsible for the elevation of blood pressure in these animals.</description><identifier>ISSN: 0022-0795</identifier><identifier>EISSN: 1479-6805</identifier><identifier>DOI: 10.1677/joe.1.06506</identifier><identifier>PMID: 16522724</identifier><identifier>CODEN: JOENAK</identifier><language>eng</language><publisher>Colchester: BioScientifica</publisher><subject>Acetylcholine - pharmacology ; Aldosterone - blood ; Angiotensin II - pharmacology ; Animals ; Animals, Newborn ; Aorta - drug effects ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Corticosterone - blood ; Dexamethasone - pharmacology ; Dose-Response Relationship, Drug ; Experimental diseases ; Female ; Glucocorticoids - pharmacology ; Hypertension - embryology ; Hypertension - pathology ; Hypertension - physiopathology ; In Vitro Techniques ; Infusion Pumps ; Medical sciences ; Mesenteric Arteries - drug effects ; Mesenteric Arteries - pathology ; Pregnancy ; Prenatal Exposure Delayed Effects ; Rats ; Rats, Wistar ; Regular papers ; Renin - blood ; Vasoconstriction - drug effects</subject><ispartof>Journal of endocrinology, 2006-03, Vol.188 (3), p.435-442</ispartof><rights>2006 Society for Endocrinology</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b439t-ec13ef4ecd3c8ed878b6773d2e8acf2ddd02801854b39d74862d450a259eb2083</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17594967$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16522724$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hadoke, P W F</creatorcontrib><creatorcontrib>Lindsay, R S</creatorcontrib><creatorcontrib>Seckl, J R</creatorcontrib><creatorcontrib>Walker, B R</creatorcontrib><creatorcontrib>Kenyon, C J</creatorcontrib><title>Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure</title><title>Journal of endocrinology</title><addtitle>J Endocrinol</addtitle><description>Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. The mechanisms underlying this programmed elevation of blood pressure have not been established. We hypothesised that prenatal glucocorticoid exposure may lead to vascular dysfunction in adulthood. Pregnant rats received dexamethasone (Dex) (100 μg/kg, s.c.) or vehicle (control) daily throughout pregnancy. Blood pressure was elevated (students t-test, unpaired; P < 0.05) in adult female offspring (aged 12–16 weeks) of Dex-treated mothers (148.0 ± 3.6 mmHg, n=10) compared with the control group (138.0 ± 2.5 mmHg, n=8). Vascular responsiveness in aortae and mesenteric arteries was differentially affected by prenatal Dex: aortae were less responsive to angiotensin II, whereas mesenteric arteries were more responsive to norepinephrine, vasopressin and potassium (mesenteric arteries respond poorly to angiotensin II in vitro). Acetylcholine-mediated, endothelium-dependent relaxation was similar in both groups. Prenatal exposure to Dex had no effect on blood pressure or aldosterone response to acute (15 min, i.v.) infusion of angiotensin II (75 ng/kg per min). In contrast, chronic (2-week, s.c.) infusion of angiotensin II (100 ng/kg per min) produced a greater elevation (P < 0.05) of blood pressure in Dex-treated rats (150.0 ± 3.6 mmHg) than in controls (135.3 ± 5.4 mmHg), and aldosterone levels were higher in Dex-treated animals. There was no angiotensin II-induced medial hypertrophy/hyperplasia in mesenteric arteries from Dex-treated rats. These results indicate that vascular function is altered in a region-specific manner in rats with glucocorticoid-programmed hypertension. Despite a striking increase in mesenteric artery contraction in Dex-treated rats, in vivo studies suggest that abnormalities of the renin-angiotensin-aldosterone system, rather than enhanced vascular contractility, may be responsible for the elevation of blood pressure in these animals.</description><subject>Acetylcholine - pharmacology</subject><subject>Aldosterone - blood</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Aorta - drug effects</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Corticosterone - blood</subject><subject>Dexamethasone - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Experimental diseases</subject><subject>Female</subject><subject>Glucocorticoids - pharmacology</subject><subject>Hypertension - embryology</subject><subject>Hypertension - pathology</subject><subject>Hypertension - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Infusion Pumps</subject><subject>Medical sciences</subject><subject>Mesenteric Arteries - drug effects</subject><subject>Mesenteric Arteries - pathology</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Regular papers</subject><subject>Renin - blood</subject><subject>Vasoconstriction - drug effects</subject><issn>0022-0795</issn><issn>1479-6805</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFLHDEUh0NpqavtqXfJpb3IbJPMZJI5ilQrCF7qOWSSN7uRzGRNMur-92bdBUGop8eD7_3eex9CPyhZ0laI3_cBlnRJWk7aT2hBG9FVrST8M1oQwlhFRMeP0HFK94RQTkX9FR3RljMmWLNA-dxniGDxo05m9jpiE6YctcnOu7zFbsLazj7jAUbtAUedE35yeY3X2w3EDFNyYcKbGFZRj2MJ6relg0ln7fHKzyaYELMzwVkMz5uQ5gjf0JdB-wTfD_UE3V3--Xfxt7q5vbq-OL-p-qbucgWG1jA0YGxtJFgpZF_-rS0Dqc3ArLWESUIlb_q6s6KRLbMNJ5rxDnpGZH2Cfu1zy3kPM6SsRpcMeK8nCHNSu7QiRBTwbA-aGFKKMKhNdKOOW0WJ2klWRbKi6lVyoU8PsXNfPn5jD1YL8PMAFKnaD1FPxqU3TvCu6drdWrbn1m61fnIRVO9CMg6m7AZn9H-20_3QO_aji18A0vup0w</recordid><startdate>20060301</startdate><enddate>20060301</enddate><creator>Hadoke, P W F</creator><creator>Lindsay, R S</creator><creator>Seckl, J R</creator><creator>Walker, B R</creator><creator>Kenyon, C J</creator><general>BioScientifica</general><general>Portland Press</general><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>7X8</scope></search><sort><creationdate>20060301</creationdate><title>Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure</title><author>Hadoke, P W F ; Lindsay, R S ; Seckl, J R ; Walker, B R ; Kenyon, C J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b439t-ec13ef4ecd3c8ed878b6773d2e8acf2ddd02801854b39d74862d450a259eb2083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Aldosterone - blood</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Aorta - drug effects</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Corticosterone - blood</topic><topic>Dexamethasone - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Experimental diseases</topic><topic>Female</topic><topic>Glucocorticoids - pharmacology</topic><topic>Hypertension - embryology</topic><topic>Hypertension - pathology</topic><topic>Hypertension - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Infusion Pumps</topic><topic>Medical sciences</topic><topic>Mesenteric Arteries - drug effects</topic><topic>Mesenteric Arteries - pathology</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Regular papers</topic><topic>Renin - blood</topic><topic>Vasoconstriction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hadoke, P W F</creatorcontrib><creatorcontrib>Lindsay, R S</creatorcontrib><creatorcontrib>Seckl, J R</creatorcontrib><creatorcontrib>Walker, B R</creatorcontrib><creatorcontrib>Kenyon, C J</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Journal of endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hadoke, P W F</au><au>Lindsay, R S</au><au>Seckl, J R</au><au>Walker, B R</au><au>Kenyon, C J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure</atitle><jtitle>Journal of endocrinology</jtitle><addtitle>J Endocrinol</addtitle><date>2006-03-01</date><risdate>2006</risdate><volume>188</volume><issue>3</issue><spage>435</spage><epage>442</epage><pages>435-442</pages><issn>0022-0795</issn><eissn>1479-6805</eissn><coden>JOENAK</coden><abstract>Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. The mechanisms underlying this programmed elevation of blood pressure have not been established. We hypothesised that prenatal glucocorticoid exposure may lead to vascular dysfunction in adulthood. Pregnant rats received dexamethasone (Dex) (100 μg/kg, s.c.) or vehicle (control) daily throughout pregnancy. Blood pressure was elevated (students t-test, unpaired; P < 0.05) in adult female offspring (aged 12–16 weeks) of Dex-treated mothers (148.0 ± 3.6 mmHg, n=10) compared with the control group (138.0 ± 2.5 mmHg, n=8). Vascular responsiveness in aortae and mesenteric arteries was differentially affected by prenatal Dex: aortae were less responsive to angiotensin II, whereas mesenteric arteries were more responsive to norepinephrine, vasopressin and potassium (mesenteric arteries respond poorly to angiotensin II in vitro). Acetylcholine-mediated, endothelium-dependent relaxation was similar in both groups. Prenatal exposure to Dex had no effect on blood pressure or aldosterone response to acute (15 min, i.v.) infusion of angiotensin II (75 ng/kg per min). In contrast, chronic (2-week, s.c.) infusion of angiotensin II (100 ng/kg per min) produced a greater elevation (P < 0.05) of blood pressure in Dex-treated rats (150.0 ± 3.6 mmHg) than in controls (135.3 ± 5.4 mmHg), and aldosterone levels were higher in Dex-treated animals. There was no angiotensin II-induced medial hypertrophy/hyperplasia in mesenteric arteries from Dex-treated rats. These results indicate that vascular function is altered in a region-specific manner in rats with glucocorticoid-programmed hypertension. Despite a striking increase in mesenteric artery contraction in Dex-treated rats, in vivo studies suggest that abnormalities of the renin-angiotensin-aldosterone system, rather than enhanced vascular contractility, may be responsible for the elevation of blood pressure in these animals.</abstract><cop>Colchester</cop><pub>BioScientifica</pub><pmid>16522724</pmid><doi>10.1677/joe.1.06506</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-0795 |
| ispartof | Journal of endocrinology, 2006-03, Vol.188 (3), p.435-442 |
| issn | 0022-0795 1479-6805 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67731737 |
| source | MEDLINE; EZB Electronic Journals Library |
| subjects | Acetylcholine - pharmacology Aldosterone - blood Angiotensin II - pharmacology Animals Animals, Newborn Aorta - drug effects Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Corticosterone - blood Dexamethasone - pharmacology Dose-Response Relationship, Drug Experimental diseases Female Glucocorticoids - pharmacology Hypertension - embryology Hypertension - pathology Hypertension - physiopathology In Vitro Techniques Infusion Pumps Medical sciences Mesenteric Arteries - drug effects Mesenteric Arteries - pathology Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Wistar Regular papers Renin - blood Vasoconstriction - drug effects |
| title | Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T17%3A07%3A45IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Altered%20vascular%20contractility%20in%20adult%20female%20rats%20with%20hypertension%20programmed%20by%20prenatal%20glucocorticoid%20exposure&rft.jtitle=Journal%20of%20endocrinology&rft.au=Hadoke,%20P%20W%20F&rft.date=2006-03-01&rft.volume=188&rft.issue=3&rft.spage=435&rft.epage=442&rft.pages=435-442&rft.issn=0022-0795&rft.eissn=1479-6805&rft.coden=JOENAK&rft_id=info:doi/10.1677/joe.1.06506&rft_dat=%3Cproquest_cross%3E67731737%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=67731737&rft_id=info:pmid/16522724&rfr_iscdi=true |