Aperia A
Department of Women and Child Health, Karolinska Institutet, 171 76 Stockholm, Sweden.
Curr Hypertens Rep. 2001 Apr;3(2):165-71. doi: 10.1007/s11906-001-0032-8.
Na+,K+-ATPase distributes ions between the intracellular and extracellular space and is responsible for total-body sodium homeostasis. The activity of this ion pump is regulated by catecholamines and peptide hormones; by the ligand of Na+,K+-ATPase, ouabain; and by direct interaction with cytoskeleton proteins. This review summarizes recent advances in the field of short-term regulation of Na+,K+-ATPase and the implications of these advances for the regulation of blood pressure. Renal Na+,K+-ATPase activity is bidirectionally regulated by natriuretic and antinatriuretic hormones, and a shift in the balance between these forces may lead to salt retention and hypertension. Dopamine plays a key role in this interactive regulation. By inhibiting vascular Na+,K+-ATPase activity, an excess of circulating ouabain may increase calcium concentration in vascular cells and lead to increased vascular contractility. Finally, mutations in cytoskeleton proteins may stimulate renal Na+,K+-ATPase activity by way of protein/protein interaction and lead to salt retention and hypertension. Abnormalities in the systems regulating Na+,K+-ATPase should be explored further in the search for the multiple causes of essential hypertension.
钠钾ATP酶在细胞内和细胞外空间之间分配离子，负责全身钠稳态。这种离子泵的活性受儿茶酚胺和肽类激素调节；受钠钾ATP酶的配体哇巴因调节；还受与细胞骨架蛋白的直接相互作用调节。本综述总结了钠钾ATP酶短期调节领域的最新进展以及这些进展对血压调节的影响。肾钠钾ATP酶活性受利钠和抗利钠激素双向调节，这些力量之间平衡的改变可能导致钠潴留和高血压。多巴胺在这种相互作用调节中起关键作用。循环中过量的哇巴因通过抑制血管钠钾ATP酶活性，可能会增加血管细胞中的钙浓度并导致血管收缩性增强。最后，细胞骨架蛋白的突变可能通过蛋白质/蛋白质相互作用刺激肾钠钾ATP酶活性，导致钠潴留和高血压。在寻找原发性高血压的多种病因时，应进一步探索调节钠钾ATP酶的系统异常情况。
