Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/103534
Type: Artigo de periódico
Title: Enhanced Calcium Mobilization In Rat Ventricular Myocytes During The Onset Of Pressure Overload-induced Hypertrophy
Author: Carvalho B.M.R.
Bassani R.A.
Franchini K.G.
Bassani J.W.M.
Abstract: Early cardiovascular changes evoked by pressure overload (PO) may reveal adaptive strategies that allow immediate survival to the increased hemodynamic load. In this study, systolic and diastolic Ca 2+ cycling was analyzed in left ventricular rat myocytes before (day 2, PO-2d group) and after (day 7, PO-7d group) development of hypertrophy subsequent to aortic constriction, as well as in myocytes from timematched sham-operated rats (sham group). Ca 2+ transient amplitude was significantly augmented in the PO-2d group. In the PO-7d group, intracellular Ca 2+ concentration ([Ca 2+] i) was reduced during diastole, and mechanical twitch relaxation (but not [Ca 2+] i decline) was slowed. In PO groups, fractional sarcoplasmic reticulum (SR) Ca 2+ release at a twitch, SR Ca 2+ content, SR Ca 2+ loss during diastole, and SR-dependent integrated Ca 2+ flux during twitch relaxation were significantly greater than in sham-operated groups, whereas the relaxation-associated Ca 2+ flux carried by the Na +/Ca 2+ exchanger was not significantly changed. In the PO-7d group, mRNA levels of cardiac isoforms of SR Ca 2+-ATPase (SERCA2a), phospholamban, calsequestrin, ryanodine receptor, and NCX were not significantly altered, but the SERCA2a-to-phospholamban ratio was increased 2.5-fold. Moreover, greater sensitivity to the inotropic effects of the β-adrenoceptor agonist isoproterenol was observed in the PO-7d group. The results indicate enhanced Ca 2+ cycling between SR and cytosol early after PO imposition, even before hypertrophy development. Increase in SR Ca 2+ uptake may contribute to enhancement of excitation-contraction coupling (augmented SR Ca 2+ content and release) and protection against arrhythmogenesis due to buildup of [Ca 2+] i during diastole. Copyright © 2006 the American Physiological Society.
Editor: 
Rights: fechado
Identifier DOI: 10.1152/ajpheart.01345.2005
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-33749362362&partnerID=40&md5=6ab1df0b02e16e964f52bc29ffec2b39
Date Issue: 2006
Appears in Collections:Unicamp - Artigos e Outros Documentos

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