Abstract Transgenic mice that overexpress human type 1 angiotensin II receptor (AT 1 R) in the heart develop cardiac hypertrophy. Previously, we have shown that in 6-mo AT 1 R mice, which exhibit significant cardiac remodeling, fractional shortening is decreased. However, it is not clear whether altered contractility is attributable to AT 1 R overexpression or is secondary to cardiac hypertrophy/remodeling. Thus the present study characterized the effects of AT 1 R overexpression on ventricular L-type Ca 2+ currents ( I CaL ), cell shortening, and Ca 2+ handling in 50-day and 6-mo-old male AT 1 R mice. Echocardiography showed there was no evidence of cardiac hypertrophy in 50-day AT 1 R mice but that fractional shortening was decreased. Cellular experiments showed that cell shortening, I CaL , and Ca v 1.2 mRNA expression were significantly reduced in 50-day and 6-mo-old AT 1 R mice compared with controls. In addition, Ca 2+ transients and caffeine-induced Ca 2+ transients were reduced whereas the time to 90% Ca 2+ transient decay was prolonged in both age groups of AT 1 R mice. Western blot analysis revealed that sarcoplasmic reticulum Ca 2+ -ATPase and Na + /Ca 2+ exchanger protein expression was significantly decreased in 50-day and 6-mo AT 1 R mice. Overall, the data show that cardiac contractility and the mechanisms that underlie excitation-contraction coupling are altered in AT 1 R mice. Furthermore, since the alterations in contractility occur before the development of cardiac hypertrophy, it is likely that these changes are attributable to the increased activity of the renin-angiotensin system brought about by AT 1 R overexpression. Thus it is possible that AT 1 R blockade may help maintain cardiac contractility in individuals with heart disease. calcium ventricle calcium current calcium transient calcium handling cardiac contraction Copyright © 2011 the American Physiological Society « Previous | Next Article » Table of Contents This Article Published online before print August 2011 , doi: 10.​1152/​ajpheart.​01092.​2010 AJP - Heart November 2011 vol. 301 no. 5 H2018-H2027 » Abstract Free Full Text Free to you Full Text (PDF) Free to you All Versions of this Article: ajpheart.01092.2010v1 301/5/H2018 most recent Classifications Cardiac Excitation and Contraction Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Download to citation manager Citing Articles Load citing article information Citing articles via Web of Science Google Scholar Articles by Rivard, K. Articles by Fiset, C. PubMed PubMed citation Articles by Rivard, K. Articles by Fiset, C. Related Content Cardiac Excitation and Contraction Load related web page information Current Issue November 2011, 301 (5) Alert me to new issues of AJP - Heart About the Journal Information for Authors Submit a Manuscript Ethical Policies AuthorChoice PubMed Central Policy Reprints and Permissions Advertising Press Copyright © 2011 the American Physiological Society Print ISSN: 0363-6135 Online ISSN: 1522-1539 var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); var pageTracker = _gat._getTracker("UA-2924550-1"); pageTracker._trackPageview();

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