{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,31]],"date-time":"2025-12-31T08:41:05Z","timestamp":1767170465488,"version":"build-2238731810"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2009,7,2]]},"abstract":"<jats:p>\n                    Cardiac hypertrophy is associated with alterations in cardiomyocyte excitation\u2013contraction coupling (ECC) and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    handling. Chronic elevation of plasma angiotensin II (Ang II) is a major determinant in the pathogenesis of cardiac hypertrophy and congestive heart failure. However, the molecular mechanisms by which the direct actions of Ang II on cardiomyocytes contribute to ECC remodeling are not precisely known. This question was addressed using cardiac myocytes isolated from transgenic (TG1306\/1R [TG]) mice exhibiting cardiac specific overexpression of angiotensinogen, which develop Ang II\u2013mediated cardiac hypertrophy in the absence of hemodynamic overload. Electrophysiological techniques, photolysis of caged Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and confocal Ca\n                    <jats:sup>2+<\/jats:sup>\n                    imaging were used to examine ECC remodeling at early (\u224820 weeks of age) and late (\u224860 weeks of age) time points during the development of cardiac dysfunction. In young TG mice, increased cardiac Ang II levels induced a hypertrophic response in cardiomyocyte, which was accompanied by an adaptive change of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling, specifically an upregulation of the Na\n                    <jats:sup>+<\/jats:sup>\n                    \/Ca\n                    <jats:sup>2+<\/jats:sup>\n                    exchanger\u2013mediated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    transport. In contrast, maladaptation was evident in older TG mice, as suggested by reduced sarcoplasmic reticulum Ca\n                    <jats:sup>2+<\/jats:sup>\n                    content resulting from a shift in the ratio of plasmalemmal Ca\n                    <jats:sup>2+<\/jats:sup>\n                    removal and sarcoplasmic reticulum Ca\n                    <jats:sup>2+<\/jats:sup>\n                    uptake. This was associated with a conserved ECC gain, consistent with a state of hypersensitivity in Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release. Together, our data suggest that chronic elevation of cardiac Ang II levels significantly alters cardiomyocyte ECC in the long term, and thereby contractility, independently of hemodynamic overload and arterial hypertension.\n                  <\/jats:p>","DOI":"10.1161\/circresaha.108.189779","type":"journal-article","created":{"date-parts":[[2009,5,28]],"date-time":"2009-05-28T21:54:54Z","timestamp":1243547694000},"page":"42-50","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":23,"title":["Angiotensin II\u2013Mediated Adaptive and Maladaptive Remodeling of Cardiomyocyte Excitation\u2013Contraction Coupling"],"prefix":"10.1161","volume":"105","author":[{"given":"Konstantin","family":"Gusev","sequence":"first","affiliation":[{"name":"From the Department of Physiology (K.G., E.N., M.E.), University of Bern, Switzerland; Department of Medicine (A.A.D., T.P.), University of Lausanne, Centre Hospitalier Universitaire Vaudois, Switzerland; and Department of Physiology (L.M.D.D.), University of Melbourne, Australia. Present address for A.A.D.: Department of Medicine, University of California at San Diego, La Jolla."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrea A.","family":"Domenighetti","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (K.G., E.N., M.E.), University of Bern, Switzerland; Department of Medicine (A.A.D., T.P.), University of Lausanne, Centre Hospitalier Universitaire Vaudois, Switzerland; and Department of Physiology (L.M.D.D.), University of Melbourne, Australia. Present address for A.A.D.: Department of Medicine, University of California at San Diego, La Jolla."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lea M.D.","family":"Delbridge","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (K.G., E.N., M.E.), University of Bern, Switzerland; Department of Medicine (A.A.D., T.P.), University of Lausanne, Centre Hospitalier Universitaire Vaudois, Switzerland; and Department of Physiology (L.M.D.D.), University of Melbourne, Australia. Present address for A.A.D.: Department of Medicine, University of California at San Diego, La Jolla."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thierry","family":"Pedrazzini","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (K.G., E.N., M.E.), University of Bern, Switzerland; Department of Medicine (A.A.D., T.P.), University of Lausanne, Centre Hospitalier Universitaire Vaudois, Switzerland; and Department of Physiology (L.M.D.D.), University of Melbourne, Australia. Present address for A.A.D.: Department of Medicine, University of California at San Diego, La Jolla."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ernst","family":"Niggli","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (K.G., E.N., M.E.), University of Bern, Switzerland; Department of Medicine (A.A.D., T.P.), University of Lausanne, Centre Hospitalier Universitaire Vaudois, Switzerland; and Department of Physiology (L.M.D.D.), University of Melbourne, Australia. Present address for A.A.D.: Department of Medicine, University of California at San Diego, La Jolla."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marcel","family":"Egger","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (K.G., E.N., M.E.), University of Bern, Switzerland; Department of Medicine (A.A.D., T.P.), University of Lausanne, Centre Hospitalier Universitaire Vaudois, Switzerland; and Department of Physiology (L.M.D.D.), University of Melbourne, Australia. Present address for A.A.D.: Department of Medicine, University of California at San Diego, La Jolla."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature06798"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200001203420301"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9149(99)00259-3"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.0000173069.53699.d9"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.73.3.8348686"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200018090-00017"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00287.2006"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.31.6.1324"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00259.2007"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.1.215"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.276.5313.800"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1387.061"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.85.11.1009"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.84.5.562"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00525.2006"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.87.8.641"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2006.09.019"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1006\/phrs.1999.0654"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2000.t01-1-00353.x"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.113910"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00015.2007"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.62.3.2449296"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2002.034728"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.2002.2037"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-0436.2001.690107.x"},{"key":"e_1_3_3_26_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.res.0000032490.04207.bd"},{"key":"e_1_3_3_27_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00393.2007"},{"key":"e_1_3_3_28_2","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvm038"},{"key":"e_1_3_3_29_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.res.0000031384.55006.db"},{"key":"e_1_3_3_30_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80847-8"},{"key":"e_1_3_3_31_2","first-page":"e65","volume":"10","year":"2008","unstructured":"Bridge JHB, Savio-Galimberti E. What are the consequences of phosphorylation and hyperphosphorylation of ryanodine receptors in normal and failing heart? 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