Contribution of Ca super(2+) transporters to relaxation in intact ventricular myocytes from developing rats

• Published in: American journal of physiology. Heart and circulatory physiology 2002-06, Vol.282 (6), p.H2406-H2413
• Main Authors: Bassani, R A, Bassani, JWM
• Format: Article
• Language: English
• ISSN: 0363-6135
• DOI: 10.1152/ajpheart.00320.2001

The relative contributions of Ca super(2+) transporters to intracellular Ca super(2+) concentration ([Ca super(2+)] sub(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 Ca super(2+) fluxes with the use of kinetic parameters calculated from [Ca super(2+)] sub(i) measurements during twitches and caffeine-evoked contractures, and from myocardial passive Ca super(2+) buffering data. Our main findings were the following: 1) twitch relaxation and [Ca super(2+)] sub(i) decline were significantly slower during the first postnatal week than in adults, 2) inhibition of sarcoplasmic reticulum (SR) Ca super(2+) accumulation resulted in faster [Ca super(2+)] sub(i) decline in young cells than in adult cells, 3) the contributions of the SR Ca super(2+) uptake and Na super(+)/Ca super(2+) exchange (NCX) to twitch relaxation increased from similar to 75 to 92%, and decreased from 24 to 5%, respectively, from birth to adulthood, and 4) Ca super(2+) transport by the sarcolemmal Ca super(2+)-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 Ca super(2+)-ATPase appears to be the predominant transporter responsible for relaxation-associated [Ca super(2+)] sub(i) decline from birth to adulthood.