Regulation of sodium/potassium ATPase activity: impact on salt balance and vascular contractility.
Regulation of sodium/potassium ATPase activity: impact on salt balance and vascular contractility.
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DOI：
10.1007/s11906-001-0032-8
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发表时间：
2001-04-01
影响因子：
5.6
通讯作者：
Aperia, A
中科院分区：
文献类型：
--
作者：
Aperia, A
Na+，K+-ATP酶在细胞内和细胞外空间之间分配离子，并负责全身钠稳态。该离子泵的活性受儿茶酚胺和肽激素、Na+，K+-ATP酶的配体哇巴因以及与细胞骨架蛋白的直接相互作用的调节。本文综述了近年来Na+，K+-ATP酶短期调节的研究进展及其对血压调节的意义。肾脏Na+，K+-ATP酶活性受利钠和抗利尿激素的双向调节，这些力量之间的平衡变化可能导致盐潴留和高血压。多巴胺在这种相互调节中起着关键作用。通过抑制血管Na+，K+-ATP酶活性，过量的循环哇巴因可增加血管细胞中的钙浓度并导致血管收缩性增加。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脏Na+，K+-ATP酶活性，并导致盐潴留和高血压。Na+，K+-ATP酶调节系统的异常在原发性高血压多病因研究中值得进一步探讨。
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.