Renin-angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice
Identifieur interne : 006754 ( Main/Exploration ); précédent : 006753; suivant : 006755Renin-angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice
Auteurs : Kesia Palma-Rigo [Australie, France] ; Kristy L. Jackson [Australie] ; Pamela J. Davern [Australie] ; Thu-Phuc Nguyen-Huu [Australie] ; Jean-Luc Elghozi [France] ; Geoffrey A. Head [Australie]Source :
- Journal of hypertension [ 0263-6352 ] ; 2011.
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- Pascal (Inist)
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Abstract
Objective Schlager hypertensive (BPH/2J) mice have been suggested to have high blood pressure (BP) due to an overactive sympathetic nervous system (SNS), but the contribution of the renin-angiotensin system (RAS) is unclear. In the present study, we examined the cardiovascular effects of chronically blocking the RAS in BPH/2J mice. Methods Schlager normotensive (BPN/3J, n = 6) and BPH/ 2J mice (n = 8) received the angiotensin AT1A-receptor antagonist losartan (150 mg/kg per day) in drinking water for 2 weeks. Pre-implanted telemetry devices were used to record mean arterial pressure (MAP), heart rate (HR) and locomotor activity. Results MAP was reduced by losartan treatment in BPN/3J (-23 mmHg, P<0.01) and in BPH/2J mice (-25 mmHg, P<0.001), whereas HR was increased. Losartan had little effect on initial pressor responses to feeding or to stress, but did attenuate the sustained pressor response to cage-switch stress. During the active period, the hypotension to sympathetic blockade with pentolinium was greater in BPH/ 2J than BPN/3J (suggesting neurogenic hypertension), but was not affected by losartan. During the inactive period, a greater depressor response to pentolinium was observed in losartan-treated animals. Conclusion The hypotensive actions of losartan suggest that although the RAS provides an important contribution to BP, it contributes little, if at all, to the hypertension-induced or the greater stress-induced pressor responses in Schlager mice. The effects of pentolinium suggest that the SNS is mainly responsible for hypertension in BPH/2J mice. However, the RAS inhibits sympathetic vasomotor tone during inactivity and prolongs sympathetic activation during periods of adverse stress, indicating an important sympathomodulatory role.
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Jackson</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute</s1><s2>Melbourne, Victoria</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Melbourne, Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Davern, Pamela J" sort="Davern, Pamela J" uniqKey="Davern P" first="Pamela J." last="Davern">Pamela J. Davern</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute</s1><s2>Melbourne, Victoria</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Melbourne, Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Nguyen Huu, Thu Phuc" sort="Nguyen Huu, Thu Phuc" uniqKey="Nguyen Huu T" first="Thu-Phuc" last="Nguyen-Huu">Thu-Phuc Nguyen-Huu</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute</s1><s2>Melbourne, Victoria</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Melbourne, Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Elghozi, Jean Luc" sort="Elghozi, Jean Luc" uniqKey="Elghozi J" first="Jean-Luc" last="Elghozi">Jean-Luc Elghozi</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>INSERM U 970, Centre de Recherche Cardiovasculaire</s1><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Centre de Recherche Cardiovasculaire</wicri:noRegion><wicri:noRegion>INSERM U 970, Centre de Recherche Cardiovasculaire</wicri:noRegion></affiliation><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>Université Paris Descartes</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement><settlement type="city">Paris</settlement></placeName><orgName type="university">Université Paris-Descartes</orgName></affiliation></author><author><name sortKey="Head, Geoffrey A" sort="Head, Geoffrey A" uniqKey="Head G" first="Geoffrey A." last="Head">Geoffrey A. Head</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute</s1><s2>Melbourne, Victoria</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Melbourne, Victoria</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Pharmacology, Monash University</s1><s2>Clayton, Victoria</s2><s3>AUS</s3><sZ>6 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Clayton, Victoria</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Journal of hypertension</title><title level="j" type="abbreviated">J. hypertens.</title><idno type="ISSN">0263-6352</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of hypertension</title><title level="j" type="abbreviated">J. hypertens.</title><idno type="ISSN">0263-6352</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Baroreflex</term><term>Cardiovascular disease</term><term>Hypertension</term><term>Mouse</term><term>Renin angiotensin system</term><term>Sympathetic nervous system</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Hypertension artérielle</term><term>Pathologie de l'appareil circulatoire</term><term>Système renin angiotensine</term><term>Système nerveux sympathique</term><term>Animal</term><term>Souris</term><term>Baroréflexe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective Schlager hypertensive (BPH/2J) mice have been suggested to have high blood pressure (BP) due to an overactive sympathetic nervous system (SNS), but the contribution of the renin-angiotensin system (RAS) is unclear. In the present study, we examined the cardiovascular effects of chronically blocking the RAS in BPH/2J mice. Methods Schlager normotensive (BPN/3J, n = 6) and BPH/ 2J mice (n = 8) received the angiotensin AT<sub>1A</sub>-receptor antagonist losartan (150 mg/kg per day) in drinking water for 2 weeks. Pre-implanted telemetry devices were used to record mean arterial pressure (MAP), heart rate (HR) and locomotor activity. Results MAP was reduced by losartan treatment in BPN/3J (-23 mmHg, P<0.01) and in BPH/2J mice (-25 mmHg, P<0.001), whereas HR was increased. Losartan had little effect on initial pressor responses to feeding or to stress, but did attenuate the sustained pressor response to cage-switch stress. During the active period, the hypotension to sympathetic blockade with pentolinium was greater in BPH/ 2J than BPN/3J (suggesting neurogenic hypertension), but was not affected by losartan. During the inactive period, a greater depressor response to pentolinium was observed in losartan-treated animals. Conclusion The hypotensive actions of losartan suggest that although the RAS provides an important contribution to BP, it contributes little, if at all, to the hypertension-induced or the greater stress-induced pressor responses in Schlager mice. The effects of pentolinium suggest that the SNS is mainly responsible for hypertension in BPH/2J mice. However, the RAS inhibits sympathetic vasomotor tone during inactivity and prolongs sympathetic activation during periods of adverse stress, indicating an important sympathomodulatory role.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement><orgName><li>Université Paris-Descartes</li></orgName></list><tree><country name="Australie"><noRegion><name sortKey="Palma Rigo, Kesia" sort="Palma Rigo, Kesia" uniqKey="Palma Rigo K" first="Kesia" last="Palma-Rigo">Kesia Palma-Rigo</name></noRegion><name sortKey="Davern, Pamela J" sort="Davern, Pamela J" uniqKey="Davern P" first="Pamela J." last="Davern">Pamela J. Davern</name><name sortKey="Head, Geoffrey A" sort="Head, Geoffrey A" uniqKey="Head G" first="Geoffrey A." last="Head">Geoffrey A. Head</name><name sortKey="Head, Geoffrey A" sort="Head, Geoffrey A" uniqKey="Head G" first="Geoffrey A." last="Head">Geoffrey A. Head</name><name sortKey="Jackson, Kristy L" sort="Jackson, Kristy L" uniqKey="Jackson K" first="Kristy L." last="Jackson">Kristy L. Jackson</name><name sortKey="Nguyen Huu, Thu Phuc" sort="Nguyen Huu, Thu Phuc" uniqKey="Nguyen Huu T" first="Thu-Phuc" last="Nguyen-Huu">Thu-Phuc Nguyen-Huu</name></country><country name="France"><noRegion><name sortKey="Palma Rigo, Kesia" sort="Palma Rigo, Kesia" uniqKey="Palma Rigo K" first="Kesia" last="Palma-Rigo">Kesia Palma-Rigo</name></noRegion><name sortKey="Elghozi, Jean Luc" sort="Elghozi, Jean Luc" uniqKey="Elghozi J" first="Jean-Luc" last="Elghozi">Jean-Luc Elghozi</name><name sortKey="Elghozi, Jean Luc" sort="Elghozi, Jean Luc" uniqKey="Elghozi J" first="Jean-Luc" last="Elghozi">Jean-Luc Elghozi</name><name sortKey="Palma Rigo, Kesia" sort="Palma Rigo, Kesia" uniqKey="Palma Rigo K" first="Kesia" last="Palma-Rigo">Kesia Palma-Rigo</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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