Altered vascular function in fetal programming of hypertension
Reduced endothelium-dependent vasorelaxation partly due to loss of nitric oxide (NO) bioavailability occurs in most cases of chronic hypertension. Intrauterine nutritional deprivation has been associated with increased risk for hypertension and stroke, associated with relaxant dysfunction and decrea...
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| creator | LAMIREAU, Delphine NUYT, Anne Monique XIN HOU BERNIER, Sylvie BEAUCHAMP, Martin GOBEIL, Fernand JR LAHAIE, Isabelle VARMA, Daya R CHEMTOB, Sylvain |
| description | Reduced endothelium-dependent vasorelaxation partly due to loss of nitric oxide (NO) bioavailability occurs in most cases of chronic hypertension. Intrauterine nutritional deprivation has been associated with increased risk for hypertension and stroke, associated with relaxant dysfunction and decreased vascular compliance, but the underlying mechanisms are not known. The present studies were undertaken to investigate whether endothelial dysfunction associated with altered NO-dependent vasodilatation pathways is also observed in a model of in utero programming of hypertension.
Pregnant Wistar rats were fed a normal (18%), low (9%), or very low (6%) protein isocaloric diet during gestation. Vasomotor response of resistance cerebral microvessels ( |
| doi_str_mv | 10.1161/01.STR.0000039340.62995.F2 |
| format | Article |
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Pregnant Wistar rats were fed a normal (18%), low (9%), or very low (6%) protein isocaloric diet during gestation. Vasomotor response of resistance cerebral microvessels (<50 micro m) was studied in adult offspring of dams fed the 18% and 9% protein diets by a video imaging technique. Endothelial NOS (eNOS), soluble guanylate cyclase (sGC), and K(Ca) channel expression were measured by Western blot. NO synthase (NOS) activity was measured enzymatically as well as in situ by NADPH diaphorase staining.
Litter size and survival to adulthood were not affected by the diets. Birth weights of offspring of dams fed the 6% diet were markedly lower than those of dams fed the 9% diet, which were marginally lower than those of controls. Systolic blood pressures of adult offspring of mothers in the 6% and 9% groups were comparably greater (156+/-2 and 155+/-1 mm Hg, respectively) than that of control offspring (137+/-1 mm Hg); we therefore focused on the 9% and 18% groups. Cerebral microvessel constriction to thromboxane A(2) mimetic and dilation to carba-prostaglandin I(2) did not differ between diet groups. In contrast, vasorelaxation to the NO-dependent agents substance P and acetylcholine was diminished by 50% in low protein-exposed offspring, but eNOS expression and activity were similar between the 2 diet groups. Vasorelaxant response to the NO donor sodium nitroprusside was also decreased and was associated with reduced (by 50% to 65%) cGMP levels and sGC expression. cGMP analogues caused comparable vasorelaxation in the 2 groups. Expression of K(Ca) (another important mediator of NO action) and relaxation to the K(Ca) opener NS1619 were unchanged by antenatal diet.
Maternal protein deprivation, which leads to hypertension in the offspring, is associated with diminished NO-dependent relaxation of major organ (cerebral) microvasculature, which seems to be largely attributed to decreased sGC expression and cGMP levels. The study provides an additional explanation for abnormal vasorelaxation in nutrient-deprived subjects in utero.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.0000039340.62995.F2</identifier><identifier>PMID: 12468802</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Chronic Disease ; Cyclic GMP - analogs & derivatives ; Cyclic GMP - metabolism ; Cyclic GMP - pharmacology ; Dietary Proteins - pharmacology ; Disease Models, Animal ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiopathology ; Enzyme Inhibitors - pharmacology ; Experimental diseases ; Female ; Guanylate Cyclase ; Hypertension - etiology ; Hypertension - physiopathology ; In Vitro Techniques ; Medical sciences ; Microcirculation - drug effects ; Microcirculation - physiopathology ; Neurotransmitter Agents - pharmacology ; Nitric Oxide - metabolism ; Nitric Oxide Donors - pharmacology ; Nitric Oxide Synthase - metabolism ; Pia Mater - blood supply ; Pregnancy ; Prenatal Exposure Delayed Effects ; Protein Deficiency - physiopathology ; Rats ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors ; Receptors, Cytoplasmic and Nuclear - metabolism ; Signal Transduction - drug effects ; Soluble Guanylyl Cyclase ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology ; Vasomotor System - drug effects ; Vasomotor System - physiopathology</subject><ispartof>Stroke (1970), 2002-12, Vol.33 (12), p.2992-2998</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Dec 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c527t-99a34ff47a3b32b388286f012e7a03d3097a1563c6f7d3de81de3a3665a6c2353</citedby><cites>FETCH-LOGICAL-c527t-99a34ff47a3b32b388286f012e7a03d3097a1563c6f7d3de81de3a3665a6c2353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,3689,27931,27932</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14409501$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12468802$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LAMIREAU, Delphine</creatorcontrib><creatorcontrib>NUYT, Anne Monique</creatorcontrib><creatorcontrib>XIN HOU</creatorcontrib><creatorcontrib>BERNIER, Sylvie</creatorcontrib><creatorcontrib>BEAUCHAMP, Martin</creatorcontrib><creatorcontrib>GOBEIL, Fernand JR</creatorcontrib><creatorcontrib>LAHAIE, Isabelle</creatorcontrib><creatorcontrib>VARMA, Daya R</creatorcontrib><creatorcontrib>CHEMTOB, Sylvain</creatorcontrib><title>Altered vascular function in fetal programming of hypertension</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Reduced endothelium-dependent vasorelaxation partly due to loss of nitric oxide (NO) bioavailability occurs in most cases of chronic hypertension. Intrauterine nutritional deprivation has been associated with increased risk for hypertension and stroke, associated with relaxant dysfunction and decreased vascular compliance, but the underlying mechanisms are not known. The present studies were undertaken to investigate whether endothelial dysfunction associated with altered NO-dependent vasodilatation pathways is also observed in a model of in utero programming of hypertension.
Pregnant Wistar rats were fed a normal (18%), low (9%), or very low (6%) protein isocaloric diet during gestation. Vasomotor response of resistance cerebral microvessels (<50 micro m) was studied in adult offspring of dams fed the 18% and 9% protein diets by a video imaging technique. Endothelial NOS (eNOS), soluble guanylate cyclase (sGC), and K(Ca) channel expression were measured by Western blot. NO synthase (NOS) activity was measured enzymatically as well as in situ by NADPH diaphorase staining.
Litter size and survival to adulthood were not affected by the diets. Birth weights of offspring of dams fed the 6% diet were markedly lower than those of dams fed the 9% diet, which were marginally lower than those of controls. Systolic blood pressures of adult offspring of mothers in the 6% and 9% groups were comparably greater (156+/-2 and 155+/-1 mm Hg, respectively) than that of control offspring (137+/-1 mm Hg); we therefore focused on the 9% and 18% groups. Cerebral microvessel constriction to thromboxane A(2) mimetic and dilation to carba-prostaglandin I(2) did not differ between diet groups. In contrast, vasorelaxation to the NO-dependent agents substance P and acetylcholine was diminished by 50% in low protein-exposed offspring, but eNOS expression and activity were similar between the 2 diet groups. Vasorelaxant response to the NO donor sodium nitroprusside was also decreased and was associated with reduced (by 50% to 65%) cGMP levels and sGC expression. cGMP analogues caused comparable vasorelaxation in the 2 groups. Expression of K(Ca) (another important mediator of NO action) and relaxation to the K(Ca) opener NS1619 were unchanged by antenatal diet.
Maternal protein deprivation, which leads to hypertension in the offspring, is associated with diminished NO-dependent relaxation of major organ (cerebral) microvasculature, which seems to be largely attributed to decreased sGC expression and cGMP levels. The study provides an additional explanation for abnormal vasorelaxation in nutrient-deprived subjects in utero.</description><subject>Animals</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>Chronic Disease</subject><subject>Cyclic GMP - analogs & derivatives</subject><subject>Cyclic GMP - metabolism</subject><subject>Cyclic GMP - pharmacology</subject><subject>Dietary Proteins - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Experimental diseases</subject><subject>Female</subject><subject>Guanylate Cyclase</subject><subject>Hypertension - etiology</subject><subject>Hypertension - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Medical sciences</subject><subject>Microcirculation - drug effects</subject><subject>Microcirculation - physiopathology</subject><subject>Neurotransmitter Agents - pharmacology</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Pia Mater - blood supply</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Protein Deficiency - physiopathology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Soluble Guanylyl Cyclase</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vasomotor System - drug effects</subject><subject>Vasomotor System - physiopathology</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1LAzEQhoMotlb_giyC3nZNMkk28SAUsSoUBD_OId1NdMt-1GRX6L83q4WCc5nDPDPz8iB0QXBGiCDXmGSvby8ZHgsUMJwJqhTPFvQATQmnLGWCykM0HccpZUpN0EkI64hTkPwYTQhlQkpMp-h2XvfW2zL5NqEYauMTN7RFX3VtUrWJs72pk43vPrxpmqr9SDqXfG431ve2DRE6RUfO1MGe7foMvS_u3-4e0-Xzw9PdfJkWnOZ9qpQB5hzLDayArkBKKoXDhNrcYCgBq9wQLqAQLi-htJKUFgwIwY0oKHCYoau_uzHL12BDr5sqFLauTWu7Ieic5hwkHcGLf-C6G3wbs2mi8viWKBqhmz-o8F0I3jq98VVj_FYTrEfFGhMdFeu9Yv2rWC_G5fPdh2HV2HK_unMagcsdEJWa2nnTFlXYc4xhxTGBH447g30</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>LAMIREAU, Delphine</creator><creator>NUYT, Anne Monique</creator><creator>XIN HOU</creator><creator>BERNIER, Sylvie</creator><creator>BEAUCHAMP, Martin</creator><creator>GOBEIL, Fernand JR</creator><creator>LAHAIE, Isabelle</creator><creator>VARMA, Daya R</creator><creator>CHEMTOB, Sylvain</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20021201</creationdate><title>Altered vascular function in fetal programming of hypertension</title><author>LAMIREAU, Delphine ; NUYT, Anne Monique ; XIN HOU ; BERNIER, Sylvie ; BEAUCHAMP, Martin ; GOBEIL, Fernand JR ; LAHAIE, Isabelle ; VARMA, Daya R ; CHEMTOB, Sylvain</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c527t-99a34ff47a3b32b388286f012e7a03d3097a1563c6f7d3de81de3a3665a6c2353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</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>Chronic Disease</topic><topic>Cyclic GMP - analogs & derivatives</topic><topic>Cyclic GMP - metabolism</topic><topic>Cyclic GMP - pharmacology</topic><topic>Dietary Proteins - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Experimental diseases</topic><topic>Female</topic><topic>Guanylate Cyclase</topic><topic>Hypertension - etiology</topic><topic>Hypertension - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Medical sciences</topic><topic>Microcirculation - drug effects</topic><topic>Microcirculation - physiopathology</topic><topic>Neurotransmitter Agents - pharmacology</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Pia Mater - blood supply</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects</topic><topic>Protein Deficiency - physiopathology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors</topic><topic>Receptors, Cytoplasmic and Nuclear - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Soluble Guanylyl Cyclase</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vasomotor System - drug effects</topic><topic>Vasomotor System - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LAMIREAU, Delphine</creatorcontrib><creatorcontrib>NUYT, Anne Monique</creatorcontrib><creatorcontrib>XIN HOU</creatorcontrib><creatorcontrib>BERNIER, Sylvie</creatorcontrib><creatorcontrib>BEAUCHAMP, Martin</creatorcontrib><creatorcontrib>GOBEIL, Fernand JR</creatorcontrib><creatorcontrib>LAHAIE, Isabelle</creatorcontrib><creatorcontrib>VARMA, Daya R</creatorcontrib><creatorcontrib>CHEMTOB, Sylvain</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LAMIREAU, Delphine</au><au>NUYT, Anne Monique</au><au>XIN HOU</au><au>BERNIER, Sylvie</au><au>BEAUCHAMP, Martin</au><au>GOBEIL, Fernand JR</au><au>LAHAIE, Isabelle</au><au>VARMA, Daya R</au><au>CHEMTOB, Sylvain</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered vascular function in fetal programming of hypertension</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>33</volume><issue>12</issue><spage>2992</spage><epage>2998</epage><pages>2992-2998</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Reduced endothelium-dependent vasorelaxation partly due to loss of nitric oxide (NO) bioavailability occurs in most cases of chronic hypertension. Intrauterine nutritional deprivation has been associated with increased risk for hypertension and stroke, associated with relaxant dysfunction and decreased vascular compliance, but the underlying mechanisms are not known. The present studies were undertaken to investigate whether endothelial dysfunction associated with altered NO-dependent vasodilatation pathways is also observed in a model of in utero programming of hypertension.
Pregnant Wistar rats were fed a normal (18%), low (9%), or very low (6%) protein isocaloric diet during gestation. Vasomotor response of resistance cerebral microvessels (<50 micro m) was studied in adult offspring of dams fed the 18% and 9% protein diets by a video imaging technique. Endothelial NOS (eNOS), soluble guanylate cyclase (sGC), and K(Ca) channel expression were measured by Western blot. NO synthase (NOS) activity was measured enzymatically as well as in situ by NADPH diaphorase staining.
Litter size and survival to adulthood were not affected by the diets. Birth weights of offspring of dams fed the 6% diet were markedly lower than those of dams fed the 9% diet, which were marginally lower than those of controls. Systolic blood pressures of adult offspring of mothers in the 6% and 9% groups were comparably greater (156+/-2 and 155+/-1 mm Hg, respectively) than that of control offspring (137+/-1 mm Hg); we therefore focused on the 9% and 18% groups. Cerebral microvessel constriction to thromboxane A(2) mimetic and dilation to carba-prostaglandin I(2) did not differ between diet groups. In contrast, vasorelaxation to the NO-dependent agents substance P and acetylcholine was diminished by 50% in low protein-exposed offspring, but eNOS expression and activity were similar between the 2 diet groups. Vasorelaxant response to the NO donor sodium nitroprusside was also decreased and was associated with reduced (by 50% to 65%) cGMP levels and sGC expression. cGMP analogues caused comparable vasorelaxation in the 2 groups. Expression of K(Ca) (another important mediator of NO action) and relaxation to the K(Ca) opener NS1619 were unchanged by antenatal diet.
Maternal protein deprivation, which leads to hypertension in the offspring, is associated with diminished NO-dependent relaxation of major organ (cerebral) microvasculature, which seems to be largely attributed to decreased sGC expression and cGMP levels. The study provides an additional explanation for abnormal vasorelaxation in nutrient-deprived subjects in utero.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>12468802</pmid><doi>10.1161/01.STR.0000039340.62995.F2</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Stroke (1970), 2002-12, Vol.33 (12), p.2992-2998 |
| issn | 0039-2499 1524-4628 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Chronic Disease Cyclic GMP - analogs & derivatives Cyclic GMP - metabolism Cyclic GMP - pharmacology Dietary Proteins - pharmacology Disease Models, Animal Endothelium, Vascular - drug effects Endothelium, Vascular - physiopathology Enzyme Inhibitors - pharmacology Experimental diseases Female Guanylate Cyclase Hypertension - etiology Hypertension - physiopathology In Vitro Techniques Medical sciences Microcirculation - drug effects Microcirculation - physiopathology Neurotransmitter Agents - pharmacology Nitric Oxide - metabolism Nitric Oxide Donors - pharmacology Nitric Oxide Synthase - metabolism Pia Mater - blood supply Pregnancy Prenatal Exposure Delayed Effects Protein Deficiency - physiopathology Rats Rats, Wistar Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors Receptors, Cytoplasmic and Nuclear - metabolism Signal Transduction - drug effects Soluble Guanylyl Cyclase Vasodilation - drug effects Vasodilator Agents - pharmacology Vasomotor System - drug effects Vasomotor System - physiopathology |
| title | Altered vascular function in fetal programming of hypertension |
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