Harik S I
Proc Natl Acad Sci U S A. 1986 Jun;83(11):4067-70. doi: 10.1073/pnas.83.11.4067.
The active transport of Na+ and K+ across the blood--brain barrier by the membrane-bound enzyme Na+/K+-activated ATPase of brain microvessel endothelial cells has a major role in the maintenance of brain water and electrolyte homeostasis. To test whether the putative noradrenergic innervation of cerebral microvessels from the nucleus locus ceruleus contributes to the regulation of Na+/K+-ATPase activity of the blood--brain barrier, specific [3H]ouabain-binding studies were performed on cerebral microvessels and crude cortical membranes obtained from Wistar rats with unilateral 6-hydroxydopamine lesion of the nucleus locus ceruleus. Such lesion depleted norepinephrine by about 90% in the ipsilateral cerebral cortex without affecting the contralateral cortex. [3H]Ouabain binding to membranes of cerebral cortex and the cerebral microvessels was specific and saturable. The maximal ouabain-binding capacity in microvessels of the ipsilateral, norepinephrine-depleted, cerebral cortex was reduced by about 40%, without change in the affinity of binding. [3H]Ouabain binding to crude membrane fractions of the cerebral cortex was not significantly affected by locus ceruleus lesion. The results suggest that Na+/K+-ATPase activity of cerebral microvessels, and the consequent transport of Na+ and K+ across the blood--brain barrier, is modulated by noradrenergic innervation from the locus ceruleus.
脑微血管内皮细胞的膜结合酶钠钾激活的ATP酶对Na⁺和K⁺跨血脑屏障的主动转运在维持脑水和电解质稳态中起主要作用。为了测试来自蓝斑核的脑微血管假定的去甲肾上腺素能神经支配是否有助于调节血脑屏障的钠钾ATP酶活性，对来自单侧6-羟基多巴胺损伤蓝斑核的Wistar大鼠的脑微血管和粗制皮质膜进行了特异性的[³H]哇巴因结合研究。这种损伤使同侧大脑皮质中的去甲肾上腺素减少了约90%，而不影响对侧皮质。[³H]哇巴因与大脑皮质和脑微血管膜的结合是特异性的且可饱和的。同侧去甲肾上腺素耗竭的大脑皮质微血管中的最大哇巴因结合能力降低了约40%，而结合亲和力没有变化。[³H]哇巴因与大脑皮质粗膜组分的结合不受蓝斑核损伤的显著影响。结果表明，脑微血管的钠钾ATP酶活性以及随之而来的Na⁺和K⁺跨血脑屏障的转运受蓝斑核的去甲肾上腺素能神经支配调节。
