File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Low-dose ramipril treatment improves relaxation and calcium cycling after established cardiac hypertrophy

TitleLow-dose ramipril treatment improves relaxation and calcium cycling after established cardiac hypertrophy
Authors
KeywordsATPase
mRNA
Myocytes
Na+/Ca2+ exchanger
Protein abundance
Sarcoplasmic reticulum
Issue Date2001
Citation
American Journal of Physiology - Heart and Circulatory Physiology, 2001, v. 280 n. 3 49-3, p. H1029-H1038 How to Cite?
AbstractRapid cooling contractures were used in this study to test whether low-dose ramipril improves sarcoplasmic reticulum (SR) Ca2+ uptake and Na+/Ca2+ exchanger function in isolated hypertrophied rat myocytes. Compensated cardiac hypertrophy was induced by abdominal aortic constriction for 5 wk followed by administration of ramipril (50 μg·kg-1·day-1) or vehicle for 4 wk. Myocyte cell length and cell width were significantly (P < 0.05) increased in both hypertrophied groups (±ramipril). Myocytes were loaded with indo 1, and relaxation was investigated after rapid cooling. Hypertrophied myocyte relaxation in Na+-free/Ca2+-free solution was 63% slower (P < 0.01) and the fall in intracellular Ca2+ was 60% slower (P < 0.05) than the relaxation of control cells. After ramipril treatment both relaxation and the decline in intracellular Ca2+ returned to control rates through improved SR Ca2+-ATPase function. Relaxation in caffeine showed no change after hypertrophy; however, after ramipril treatment the time to 50% relaxation in caffeine decreased by 30% (P < 0.05). The improvement in Ca2+ extrusion across the sarcolemmal membrane occurred independently of changes in Na+/Ca2+ exchanger mRNA and protein abundance. These data demonstrate that ramipril improves both SR-dependent and non-SR-dependent calcium cycling after established cardiac hypertrophy. However, the improvements in function are independent of transcriptional activation and likely to involve altered intracellular ion concentrations.
Persistent Identifierhttp://hdl.handle.net/10722/195251
ISSN
2023 Impact Factor: 4.1
2023 SCImago Journal Rankings: 1.452
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBoateng, SY-
dc.contributor.authorNaqvi, RU-
dc.contributor.authorKoban, MU-
dc.contributor.authorYacoub, MH-
dc.contributor.authorMacLeod, KT-
dc.contributor.authorBoheler, KR-
dc.date.accessioned2014-02-25T01:40:21Z-
dc.date.available2014-02-25T01:40:21Z-
dc.date.issued2001-
dc.identifier.citationAmerican Journal of Physiology - Heart and Circulatory Physiology, 2001, v. 280 n. 3 49-3, p. H1029-H1038-
dc.identifier.issn0363-6135-
dc.identifier.urihttp://hdl.handle.net/10722/195251-
dc.description.abstractRapid cooling contractures were used in this study to test whether low-dose ramipril improves sarcoplasmic reticulum (SR) Ca2+ uptake and Na+/Ca2+ exchanger function in isolated hypertrophied rat myocytes. Compensated cardiac hypertrophy was induced by abdominal aortic constriction for 5 wk followed by administration of ramipril (50 μg·kg-1·day-1) or vehicle for 4 wk. Myocyte cell length and cell width were significantly (P < 0.05) increased in both hypertrophied groups (±ramipril). Myocytes were loaded with indo 1, and relaxation was investigated after rapid cooling. Hypertrophied myocyte relaxation in Na+-free/Ca2+-free solution was 63% slower (P < 0.01) and the fall in intracellular Ca2+ was 60% slower (P < 0.05) than the relaxation of control cells. After ramipril treatment both relaxation and the decline in intracellular Ca2+ returned to control rates through improved SR Ca2+-ATPase function. Relaxation in caffeine showed no change after hypertrophy; however, after ramipril treatment the time to 50% relaxation in caffeine decreased by 30% (P < 0.05). The improvement in Ca2+ extrusion across the sarcolemmal membrane occurred independently of changes in Na+/Ca2+ exchanger mRNA and protein abundance. These data demonstrate that ramipril improves both SR-dependent and non-SR-dependent calcium cycling after established cardiac hypertrophy. However, the improvements in function are independent of transcriptional activation and likely to involve altered intracellular ion concentrations.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiology-
dc.subjectATPase-
dc.subjectmRNA-
dc.subjectMyocytes-
dc.subjectNa+/Ca2+ exchanger-
dc.subjectProtein abundance-
dc.subjectSarcoplasmic reticulum-
dc.titleLow-dose ramipril treatment improves relaxation and calcium cycling after established cardiac hypertrophy-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid11179044-
dc.identifier.scopuseid_2-s2.0-0034972108-
dc.identifier.volume280-
dc.identifier.issue3 49-3-
dc.identifier.spageH1029-
dc.identifier.epageH1038-
dc.identifier.isiWOS:000166978000013-
dc.identifier.issnl0363-6135-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats