Jurkowitz M S, Brierley G P
J Bioenerg Biomembr. 1982 Dec;14(5-6):435-49. doi: 10.1007/BF00743069.
A rapid loss of accumulated Ca2+ is produced by addition of H+ to isolated heart mitochondria. The H+-dependent Ca+ efflux requires that either (a) the NAD(P)H pool of the mitochondrion be oxidized, or (b) the endogenous adenine nucleotides be depleted. The loss of Ca2+ is accompanied by swelling and loss of endogenous Mg2+. The rate of H+-dependent Ca2+ efflux depends on the amount of Ca2+ and Pi taken up and the extent of the pH drop imposed. In the absence of ruthenium red the H+-induced Ca2+-efflux is partially offset by a spontaneous re-accumulation of released Ca2+. The H+-induced Ca2+ efflux is inhibited when the Pi transporter is blocked with N-ethylmaleimide, is strongly opposed by oligomycin and exogenous adenine nucleotides (particularly ADP), and inhibited by nupercaine. The H+-dependent Ca2+ efflux is decreased markedly when Na+ replaces the K+ of the suspending medium or when the exogenous K+/H+ exchanger nigericin is present. These results suggest that the H+-dependent loss of accumulated Ca2+ results from relatively nonspecific changes in membrane permeability and is not a reflection of a Ca2+/H+ exchange reaction.
向分离的心脏线粒体中添加H⁺会导致积累的Ca²⁺快速流失。H⁺依赖性Ca²⁺外流要求:(a)线粒体的NAD(P)H池被氧化,或(b)内源性腺嘌呤核苷酸被耗尽。Ca²⁺的流失伴随着肿胀和内源性Mg²⁺的丧失。H⁺依赖性Ca²⁺外流的速率取决于摄取的Ca²⁺和Pi的量以及施加的pH下降程度。在没有钌红的情况下,H⁺诱导的Ca²⁺外流会被释放的Ca²⁺的自发重新积累部分抵消。当Pi转运体被N-乙基马来酰胺阻断时,H⁺诱导的Ca²⁺外流受到抑制,寡霉素和外源性腺嘌呤核苷酸(特别是ADP)强烈对抗该外流,并且奴夫卡因也能抑制该外流。当Na⁺取代悬浮介质中的K⁺或存在外源性K⁺/H⁺交换剂尼日利亚菌素时,H⁺依赖性Ca²⁺外流会显著降低。这些结果表明,H⁺依赖性积累的Ca²⁺流失是由膜通透性的相对非特异性变化引起的,而不是Ca²⁺/H⁺交换反应的反映。