Soler F, Sanchez-Migallon P, Gomez-Fernandez J C, Fernandez-Belda F
Departamento de Bioquimica y Biologia Molecular, Facultad de Veterinaria, Universidad de Murcia, Spain.
J Bioenerg Biomembr. 1994 Feb;26(1):127-36. doi: 10.1007/BF00763224.
The release of H+ during the oxalate-supported Ca2+ uptake in sarcoplasmic reticulum vesicles is kinetically coincident with the initial phase of Ca2+ accumulation. The Ca2+ uptake is increased and the H+ release is decreased in the presence of KCl and other monovalent chloride salts as expected for a H(+)-monovalent cation exchange. The functioning of the Ca(2+)-pump is disturbed by the presence of potassium gluconate and to a lesser extent, of choline chloride. These salts do not inhibit the ATPase activity of Ca(2+)-permeable vesicles, suggesting a charge imbalance inhibition which is specially relevant in the case of gluconate. Therefore, K+, and also Cl-, appear to be involved in secondary fluxes during the active accumulation of Ca2+. The microsomal preparation seems homogeneous with respect to the K(+)-channel, showing an apparent rate constant for K+ release of approximately 25 s-1 measured with the aid of 86Rb+ tracer under equilibrium conditions. A Rb+ efflux, sensitive to Ca(2+)-ionophore, can be also detected during the active accumulation of Ca2+. The experimental data suggest that both monovalent cations and anions are involved in a charge compensation during the Ca2+ uptake and H+ release. Fluxes of these highly permeable ions would contribute to cancel the formation of a resting membrane potential through the sarcoplasmic reticulum membrane.
在肌浆网囊泡中草酸盐支持的Ca2+摄取过程中，H+的释放与Ca2+积累的初始阶段在动力学上是一致的。如H(+)-单价阳离子交换所预期的那样，在KCl和其他单价氯化物盐存在的情况下，Ca2+摄取增加而H+释放减少。葡萄糖酸钾的存在会干扰Ca(2+)-泵的功能，氯化胆碱的干扰程度较小。这些盐不会抑制Ca(2+)-可渗透囊泡的ATP酶活性，这表明存在电荷失衡抑制，在葡萄糖酸盐的情况下尤其相关。因此，K+以及Cl-似乎都参与了Ca2+主动积累过程中的次级通量。微粒体制备物在K(+)-通道方面似乎是均匀的，在平衡条件下借助86Rb+示踪剂测量，K+释放的表观速率常数约为25 s-1。在Ca2+主动积累过程中也可以检测到对Ca(2+)-离子载体敏感的Rb+外流。实验数据表明，单价阳离子和阴离子在Ca2+摄取和H+释放过程中都参与了电荷补偿。这些高渗透性离子的通量将有助于抵消通过肌浆网膜形成的静息膜电位。
