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Articles in PresS, published online ahead of print January 24, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00320.2001
Submitted on April 20, 2001
Accepted on January 21, 2002
1 Centro de Engenharia Biomedica, Universidade Estadual de Campinas, Campinas, Sao Paulo, Brazil
2 Dep. Engenharia Biomedica/FEEC, Universidade Estadual de Campinas, Campinas, Sao Paulo, Brazil; Centro de Engenharia Biomedica, Universidade Estadual de Campinas, Campinas, Sao Paulo, Brazil
The relative contributions of Ca2+ transporters to [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 using kinetic parameters calculated from [Ca2+]i measurements during twitches and caffeine-evoked contractures, and from myocardial passive Ca2+ buffering data. Our main findings were: a) twitch relaxation and [Ca2+]i decline were significantly slower during the first post-natal week than in adults; b) inhibition of sarcoplasmic reticulum (SR) Ca2+ accumulation resulted in faster [Ca2+]i decline in young than in adult cells; c) 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; d) Ca2+ transport by the sarcolemmal Ca2+-ATPase was apparently increased in neonates. Our data indicate that, despite 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.
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