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Article: Sub-antihypertensive doses of ramipril normalize sarcoplasmic reticulum calcium ATPase expression and function following cardiac hypertrophy in rats

TitleSub-antihypertensive doses of ramipril normalize sarcoplasmic reticulum calcium ATPase expression and function following cardiac hypertrophy in rats
Authors
Issue Date1998
Citation
Journal of Molecular and Cellular Cardiology, 1998, v. 30 n. 12, p. 2683-2694 How to Cite?
AbstractWe examined the hypothesis that the angiotensin converting enzyme inhibitor ramipril at sub-antihypertensive concentrations could improve sarcoplasmic reticulum (SR) CaATPase expression and function in compensated hypertrophied rat hearts. Five weeks after abdominal aortic constriction, rats received a daily dose (50 μg/kg/day) of ramipril or vehicle for 4 weeks. Cardiac angiotensin-converting enzyme (ACE) activity increased with cardiac hypertrophy (CH) but returned to normal following ramipril treatment. SR CaATPase protein levels and activity decreased with CH (P < 0.05) and were normalized following ramipril treatment (P < 0.05 for protein and activity). No change in phospholamban (PLB) protein levels could be demonstrated between any of the groups. In contrast, ramipril treatment specifically increased control SR CaATPase and PLB mRNA levels by > 60% (P < 0.01) and > 30%, respectively. In the hypertrophied group, SR CaATPase increased by 35% (P < 0.05 n = 6) after ramipril treatment. Calsequestrin mRNA levels were unaffected by ramipril administration. In conclusion, ramipril normalizes SR CaATPase protein expression and function in pressure-overloaded and compensated CH. The effects of ramipril are however multifaceted, affecting RNA and protein expression differentially.
Persistent Identifierhttp://hdl.handle.net/10722/195246
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBoateng, SY-
dc.contributor.authorSeymour, A-ML-
dc.contributor.authorBhutta, NS-
dc.contributor.authorDunn, MJ-
dc.contributor.authorYacoub, MH-
dc.contributor.authorBoheler, KR-
dc.date.accessioned2014-02-25T01:40:21Z-
dc.date.available2014-02-25T01:40:21Z-
dc.date.issued1998-
dc.identifier.citationJournal of Molecular and Cellular Cardiology, 1998, v. 30 n. 12, p. 2683-2694-
dc.identifier.issn0022-2828-
dc.identifier.urihttp://hdl.handle.net/10722/195246-
dc.description.abstractWe examined the hypothesis that the angiotensin converting enzyme inhibitor ramipril at sub-antihypertensive concentrations could improve sarcoplasmic reticulum (SR) CaATPase expression and function in compensated hypertrophied rat hearts. Five weeks after abdominal aortic constriction, rats received a daily dose (50 μg/kg/day) of ramipril or vehicle for 4 weeks. Cardiac angiotensin-converting enzyme (ACE) activity increased with cardiac hypertrophy (CH) but returned to normal following ramipril treatment. SR CaATPase protein levels and activity decreased with CH (P < 0.05) and were normalized following ramipril treatment (P < 0.05 for protein and activity). No change in phospholamban (PLB) protein levels could be demonstrated between any of the groups. In contrast, ramipril treatment specifically increased control SR CaATPase and PLB mRNA levels by > 60% (P < 0.01) and > 30%, respectively. In the hypertrophied group, SR CaATPase increased by 35% (P < 0.05 n = 6) after ramipril treatment. Calsequestrin mRNA levels were unaffected by ramipril administration. In conclusion, ramipril normalizes SR CaATPase protein expression and function in pressure-overloaded and compensated CH. The effects of ramipril are however multifaceted, affecting RNA and protein expression differentially.-
dc.languageeng-
dc.relation.ispartofJournal of Molecular and Cellular Cardiology-
dc.titleSub-antihypertensive doses of ramipril normalize sarcoplasmic reticulum calcium ATPase expression and function following cardiac hypertrophy in rats-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1006/jmcc.1998.0830-
dc.identifier.pmid9990539-
dc.identifier.scopuseid_2-s2.0-0032445050-
dc.identifier.volume30-
dc.identifier.issue12-
dc.identifier.spage2683-
dc.identifier.epage2694-
dc.identifier.isiWOS:000077947500018-

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