Cancherini Douglas V, Trabuco Leonardo G, Rebouças Nancy A, Kowaltowski Alicia J
Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, Cidade Universitária, 05508-900 São Paulo, Brazil.
Am J Physiol Renal Physiol. 2003 Dec;285(6):F1291-6. doi: 10.1152/ajprenal.00103.2003. Epub 2003 Sep 2.
Isolated kidney mitochondria swell when incubated in hyposmotic solutions containing K+ salts in a manner inhibited by ATP, ADP, 5-hydroxydecanoate, and glibenclamide and stimulated by GTP and diazoxide. These results suggest the existence of ATP-sensitive K+ channels in these mitochondria, similar to those previously described in heart, liver, and brain. Renal mitochondrial ATP-sensitive K+ uptake rates are approximately 140 nmol.min-1.mg protein-1. This K+ transport results in a slight increase in respiration and decrease in the inner membrane potential. In addition, the activation of ATP-inhibited K+ uptake using diazoxide leads to a decrease of ATP hydrolysis through the reverse activity of the F0F1 ATP synthase when respiration is inhibited. In conclusion, we characterize an ATP-sensitive K+ transport pathway in kidney mitochondria that affects volume, respiration, and membrane potential and may have a role in the prevention of mitochondrial ATP hydrolysis.
分离的肾线粒体在含有钾盐的低渗溶液中孵育时会肿胀，其方式受到ATP、ADP、5-羟基癸酸盐和格列本脲的抑制，并受到GTP和二氮嗪的刺激。这些结果表明，这些线粒体中存在ATP敏感性钾通道，类似于先前在心脏、肝脏和大脑中描述的通道。肾线粒体ATP敏感性钾摄取率约为140 nmol·min⁻¹·mg蛋白质⁻¹。这种钾转运导致呼吸略有增加，内膜电位降低。此外，当呼吸受到抑制时，使用二氮嗪激活ATP抑制的钾摄取会通过F₀F₁ATP合酶的反向活性导致ATP水解减少。总之，我们描述了肾线粒体中一种ATP敏感性钾转运途径，该途径影响体积、呼吸和膜电位，可能在预防线粒体ATP水解中发挥作用。
