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Am J Physiol Heart Circ Physiol 282: H2406-H2413, 2002. First published January 24, 2002; doi:10.1152/ajpheart.00320.2001
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Vol. 282, Issue 6, H2406-H2413, June 2002

Contribution of Ca2+ transporters to relaxation in intact ventricular myocytes from developing rats

Rosana A. Bassani and José W. M. Bassani

Centro de Engenharia Biomédica and Departamento de Engenharia Biomédica/ Faculdade de Engenharia Elétrica e de Computação, Universidade Estadual de Campinas, Campinas 13083-971, Brazil

The relative contributions of Ca2+ transporters to intracellular Ca2+ concentration ([Ca2+]i) decline associated with twitch relaxation were analyzed in intact ventricular myocytes from developing and adult rats. This was accomplished by estimation of individual integrated Ca2+ fluxes with the use of kinetic parameters calculated from [Ca2+]i measurements during twitches and caffeine-evoked contractures, and from myocardial passive Ca2+ buffering data. Our main findings were the following: 1) twitch relaxation and [Ca2+]i decline were significantly slower during the first postnatal week than in adults, 2) inhibition of sarcoplasmic reticulum (SR) Ca2+ accumulation resulted in faster [Ca2+]i decline in young cells than in adult cells, 3) the contributions of the SR Ca2+ uptake and Na+/Ca2+ exchange (NCX) to twitch relaxation increased from ~75 to 92%, and decreased from 24 to 5%, respectively, from birth to adulthood, and 4) Ca2+ transport by the sarcolemmal Ca2+-ATPase was apparently increased in neonates. Our data indicate that despite a marked increase in NCX contribution to cell relaxation in immature rats, the SR Ca2+-ATPase appears to be the predominant transporter responsible for relaxation-associated [Ca2+]i decline from birth to adulthood.

sarcoplasmic reticulum Ca2+-ATPase; Na+-Ca2+ exchange; sarcolemmal Ca2+-ATPase; mitochondrial Ca2+ uniporter


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