Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation
Identifieur interne : 000769 ( Main/Exploration ); précédent : 000768; suivant : 000770Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation
Auteurs : Analia S. Loria [États-Unis, Géorgie (pays)] ; David M. Pollock [Géorgie (pays), États-Unis] ; Jennifer S. Pollock [Géorgie (pays), États-Unis]Source :
- Physiological Reports [ 2051-817X ] ; 2015.
Abstract
We previously reported that maternal separation, rat model of early life stress, enhances pressor responses to acute and chronic stressors. The aims of this study were to determine whether Dahl salt-sensitive (DS) rats subjected to maternal separation (MatSep-DS) as compared to normally reared DS (Ctl-DS) rats show exaggerated blood pressure responses to acute behavioral stressors, such as restraint stress or air jet stress (AJS), or, hypertensive stimuli including chronic high-salt diet (4% NaCl) and angiotensin II (AngII) infusion (200 ng/Kg/min) during 1 week. MatSep was performed in male DS rats for 3 h/day from postnatal days 2–14. At 8 weeks of age, rats were implanted with telemetry transmitters and allowed to recover. Mean arterial pressure (MAP) was not different between MatSep-DS and Ctl-DS rats at baseline (120 ± 2 mmHg vs. 118 ± 1 mmHg,
Url:
DOI: 10.14814/phy2.12408
PubMed: 25999404
PubMed Central: 4463836
Affiliations:
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Loria</name><affiliation wicri:level="2"><nlm:aff id="au1"><institution>Department of Pharmacology and Nutritional Sciences, University of Kentucky</institution><addr-line>Lexington, Kentucky</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Lexington</wicri:cityArea></affiliation><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Department of Medicine, Georgia Regents University</institution><addr-line>Augusta, Georgia</addr-line></nlm:aff><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Augusta</wicri:regionArea></affiliation></author><author><name sortKey="Pollock, David M" sort="Pollock, David M" uniqKey="Pollock D" first="David M" last="Pollock">David M. Pollock</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Department of Medicine, Georgia Regents University</institution><addr-line>Augusta, Georgia</addr-line></nlm:aff><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Augusta</wicri:regionArea></affiliation><affiliation wicri:level="2"><nlm:aff id="au3"><institution>Cardio-Renal Physiology & Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham</institution><addr-line>Birmingham, Alabama</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Birmingham</wicri:cityArea></affiliation></author><author><name sortKey="Pollock, Jennifer S" sort="Pollock, Jennifer S" uniqKey="Pollock J" first="Jennifer S" last="Pollock">Jennifer S. Pollock</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Department of Medicine, Georgia Regents University</institution><addr-line>Augusta, Georgia</addr-line></nlm:aff><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Augusta</wicri:regionArea></affiliation><affiliation wicri:level="2"><nlm:aff id="au3"><institution>Cardio-Renal Physiology & Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham</institution><addr-line>Birmingham, Alabama</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Birmingham</wicri:cityArea></affiliation></author></analytic><series><title level="j">Physiological Reports</title><idno type="ISSN">2051-817X</idno><idno type="eISSN">2051-817X</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>We previously reported that maternal separation, rat model of early life stress, enhances pressor responses to acute and chronic stressors. The aims of this study were to determine whether Dahl salt-sensitive (DS) rats subjected to maternal separation (MatSep-DS) as compared to normally reared DS (Ctl-DS) rats show exaggerated blood pressure responses to acute behavioral stressors, such as restraint stress or air jet stress (AJS), or, hypertensive stimuli including chronic high-salt diet (4% NaCl) and angiotensin II (AngII) infusion (200 ng/Kg/min) during 1 week. MatSep was performed in male DS rats for 3 h/day from postnatal days 2–14. At 8 weeks of age, rats were implanted with telemetry transmitters and allowed to recover. Mean arterial pressure (MAP) was not different between MatSep-DS and Ctl-DS rats at baseline (120 ± 2 mmHg vs. 118 ± 1 mmHg, <italic>n</italic> = 4–8). Blood pressure responses during AJS and restraint stress were not different between MatSep-DS and Ctl-DS at 3 min. However, blood pressure recovery from AJS was significantly impaired in MatSep-DS rats compared to Ctl-DS rats (<italic>P</italic> < 0.05). 3-h stress-induced similar responses in MatSep and Ctl-DS rats. Chronic blood pressure responses to AngII infusion in rats fed a high-salt diet displayed enhanced MAP in MatSep-DS when compared with Ctl-DS rats (167 ± 5 mmHg vs. 152 ± 2 mmHg, p<sub>interaction</sub> <0.05). However, MAP increased similarly in both groups in response to AngII infusion or high-salt diet separately. Renal parameters such as proteinuria, urine flow rate, and urine electrolytes were not different between groups in response to each treatment. In summary, salt sensitivity induces exaggerated blood pressor responses only in presence of AngII due to early life stress.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Alastalo, H" uniqKey="Alastalo H">H Alastalo</name></author><author><name sortKey="Raikkonen, K" uniqKey="Raikkonen K">K Raikkonen</name></author><author><name sortKey="Pesonen, A K" uniqKey="Pesonen A">A-K Pesonen</name></author><author><name sortKey="Osmond, C" uniqKey="Osmond C">C Osmond</name></author><author><name sortKey="Barker, Djp" uniqKey="Barker D">DJP Barker</name></author><author><name sortKey="Heinonen, K" uniqKey="Heinonen K">K Heinonen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Barton, M" uniqKey="Barton M">M Barton</name></author><author><name sortKey="D Uscio, Lv" uniqKey="D Uscio L">LV d'Uscio</name></author><author><name sortKey="Shaw, S" uniqKey="Shaw S">S Shaw</name></author><author><name 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J" uniqKey="Kunes J">J Kuneš</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Géorgie (pays)</li><li>États-Unis</li></country><region><li>Alabama</li><li>Kentucky</li></region></list><tree><country name="États-Unis"><region name="Kentucky"><name sortKey="Loria, Analia S" sort="Loria, Analia S" uniqKey="Loria A" first="Analia S" last="Loria">Analia S. Loria</name></region><name sortKey="Pollock, David M" sort="Pollock, David M" uniqKey="Pollock D" first="David M" last="Pollock">David M. Pollock</name><name sortKey="Pollock, Jennifer S" sort="Pollock, Jennifer S" uniqKey="Pollock J" first="Jennifer S" last="Pollock">Jennifer S. Pollock</name></country><country name="Géorgie (pays)"><noRegion><name sortKey="Loria, Analia S" sort="Loria, Analia S" uniqKey="Loria A" first="Analia S" last="Loria">Analia S. Loria</name></noRegion><name sortKey="Pollock, David M" sort="Pollock, David M" uniqKey="Pollock D" first="David M" last="Pollock">David M. Pollock</name><name sortKey="Pollock, Jennifer S" sort="Pollock, Jennifer S" uniqKey="Pollock J" first="Jennifer S" last="Pollock">Jennifer S. Pollock</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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