Mechanisms of the modulation of Ca movement and contracti in acidosis

研究了细胞内酸化对Ca~(2+)的处理机制和张力发展的影响。CO_2酸中毒(ACD)增加了钙瞬变(CAT)，延长了其衰变时间，但张力受到抑制，但其时程变化不明显。ACD可降低破伤风制剂中接触元件的钙敏感性，抑制最大张力。ACD可降低收缩时肌肉从Lmax快速释放至92%Lmax所引起的CAT(Extra-Ca)的一过性升高，进一步提示收缩元件对钙的敏感性降低。用去皮小梁观察了H~(2+)对肌浆网(SR)Ca~(2+)处理的影响。H~+可抑制钙离子诱导的钙释放(CICR)和钙离子摄取。H^+对PCA6诱导的CICR有明显的抑制作用。ACD中CAT的增加是由于钙敏感性的降低，而酸中毒时CAT的缓慢衰退是由于SR对Ca~(2+)的缓慢摄取。

Effects of intracellular acidification on Ca^<2+> handling mechanisms and tension development were studied using intact and skinned preparations. CO_2 acidosis (ACD) increased Ca^<2+> transient (CaT) and prolonged its decay time, although tension was inhibited without a significant change of its time course. ACD decreased the Ca sensitivity of the contactile elememts and suppressed the maximal tension in tetanized-preparations. A transient increase in CaT (extra-Ca), which was induced by a quick release of muscle from Lmax to 92% Lmax during a twich contraction, was decreased by ACD.This further suggests a decrease in the Ca sensitivity of the contractile elements. The effects of H^+ on the Ca^<2+> handling of the sarcoplasmic reticulum (SR) weere examined using skinned trabeculae in which Ca^<2+> measured using the fluorescent Ca indicator, fluo-3. Ca-induced Ca release (CICR) and Ca^<2+> uptake by tge SR were all inhibited by H^+. CICR induced by pCa 6 was particularly inhibited by H^+. The increase in CaT in ACD is due to a decrease in the Ca sensitivity and the slow decay of the CaT in acidosis is due to the slow uptake of Ca^<2+> by the SR.