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首页> 外文期刊>American Journal of Physiology >Contribution of Ca(2+) transporters to relaxation in intact ventricular myocytes from developing rats.
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Contribution of Ca(2+) transporters to relaxation in intact ventricular myocytes from developing rats.

机译:Ca(2+)转运蛋白对来自发育中大鼠的完整心室肌细胞的松弛作用。

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The relative contributions of Ca(2+) transporters to intracellular Ca(2+) concentration ([Ca(2+)](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(2+) fluxes with the use of kinetic parameters calculated from [Ca(2+)](i) measurements during twitches and caffeine-evoked contractures, and from myocardial passive Ca(2+) buffering data. Our main findings were the following: 1) twitch relaxation and [Ca(2+)](i) decline were significantly slower during the first postnatal week than in adults, 2) inhibition of sarcoplasmic reticulum (SR) Ca(2+) accumulation resulted in faster [Ca(2+)](i) decline in young cells than in adult cells, 3) the contributions of the SR Ca(2+) uptake and Na(+)/Ca(2+) exchange (NCX) to twitch relaxation increased from ~75 to 92%, and decreased from 24 to 5%, respectively, from birth to adulthood, and 4) Ca(2+) transport by the sarcolemmal Ca(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(2+)-ATPase appears to be the predominant transporter responsible for relaxation-associated [Ca(2+)](i) decline from birth to adulthood.
机译:在发育和成年大鼠的完整心室肌细胞中分析了Ca(2+)转运蛋白对细胞内Ca(2+)浓度([Ca(2 +)](i))下降与抽动弛豫相关的相对贡献。这是通过在抽搐和咖啡因诱发的挛缩过程中,从[Ca(2 +)](i)测量值和心肌被动Ca(2+)计算得出的动力学参数估算单个积分Ca(2+)通量来完成的缓冲数据。我们的主要发现如下:1)产后第一周的抽搐松弛和[Ca(2 +)](i)下降明显慢于成人,2)抑制肌浆网(SR)Ca(2+)积累导致年轻细胞中的[Ca(2 +)](i)下降速度快于成年细胞,3)SR Ca(2+)摄取和Na(+)/ Ca(2+)交换(NCX)的贡献从出生到成年,抽搐放松从〜75%增加到92%,从24%减少到5%,并且4)肌膜Ca(2 + -ATPase)的Ca(2+)转运在新生儿中明显增加。我们的数据表明,尽管NCX对未成熟大鼠的细胞松弛的贡献显着增加,但SR Ca(2 +)-ATPase似乎是导致与松弛相关的[Ca(2 +)](i)从生于成年。

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