William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, London, UK.
Centre for Cardiovascular and Metabolic Neuroscience, Neuroscience, Physiology & Pharmacology, University College London, London, UK.
J Cereb Blood Flow Metab. 2019 Oct;39(10):2089-2095. doi: 10.1177/0271678X18780602. Epub 2018 Jun 4.
K6.1 (KCNJ8) is a subunit of ATP sensitive potassium channel (K) that plays an important role in the control of peripheral vascular tone and is highly expressed in brain contractile cells (vascular smooth muscle cells and pericytes). This study determined the effect of global deletion of the K6.1 subunit on cerebral blood flow, neurovascular coupling and cerebral oxygenation in mice. In K6.1 deficient mice resting cerebral blood flow and brain parenchymal partial pressure of oxygen (O) were found to be markedly lower compared to that in their wildtype littermates. However, cortical blood oxygen level dependent responses triggered by visual stimuli were not affected in conditions of K6.1 deficiency. These data suggest that K channels containing K6.1 subunit are critically important for the maintenance of normal cerebral perfusion and parenchymal O but play no significant role in the mechanisms underlying functional changes in brain blood flow.
K6.1(KCNJ8)是 ATP 敏感性钾通道(K)的一个亚基,在调节外周血管张力方面发挥着重要作用,并且在大脑收缩细胞(血管平滑肌细胞和周细胞)中高度表达。本研究旨在确定 K6.1 亚基的全局缺失对小鼠脑血流、神经血管耦合和脑氧合的影响。研究发现,与野生型同窝仔相比,K6.1 缺陷型小鼠的静息脑血流和脑实质氧分压(O2)明显降低。然而,在 K6.1 缺乏的情况下,视觉刺激引发的皮质血氧水平依赖性反应不受影响。这些数据表明,含有 K6.1 亚基的 K 通道对于维持正常脑灌注和实质 O2至关重要,但在脑血流功能变化的机制中没有发挥重要作用。