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首页> 外文期刊>American Journal of Physiology >ROMK is required for expression of the 70-pS K channel in the thick ascending limb.
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ROMK is required for expression of the 70-pS K channel in the thick ascending limb.

机译：在厚的上升肢中表达70-pS K通道需要ROMK。

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摘要

Apical potassium recycling is crucial for salt transport by the thick ascending limb (TAL). Loss-of-function mutations in the K channel, ROMK (Kir1.1; KCNJ1), cause Bartter syndrome, a genetically heterogeneous disorder characterized by severe reduction in salt absorption by the TAL, Na wasting, polyuria, and hypokalemic alkalosis. ROMK(-/-) null mice exhibit a Bartter phenotype and lack the small-conductance (30-pS) apical K channel (SK) in the TAL. However, a distinct 70-pS K channel can also significantly contribute to the apical conductance of TAL. We now examine the effect of ROMK deletion on the functional expression of the 70-pS K channel in the TAL. Functional expression of the 70-pS K channel was low [average channel activity (NP(o)) = 0.02] in ROMK(+/+) mice on a control K diet but increased to 0.27 by high-K intake for 2 wk. In contrast, the high-K diet decreased NP(o) of SK by approximately 30%, from 2.04 to 1.44. In ROMK heterozygous (+/-) mice on a control K diet, SK activity was about one-half of that observed in ROMK(+/+) mice (0.95 vs. 2.04). The high-K diet also reduced SK activity in ROMK(+/-) mice by approximately 40% (from 0.95 to 0.55) but increased NP(o) of the 70-pS K channel from 0 to 0.09 in ROMK(+/-) mice. This corresponds to approximately 30% of channel activity (NP(o) = 0.27) observed in ROMK(+/+) mice. Neither the 70-pS nor the 30-pS K channels were observed in TAL cells from ROMK(-/-) mice on either the normal or high-K diets. Thus functional expression of the 70-pS K channel is enhanced by increasing dietary K and requires expression of ROMK. It is likely that ROMK forms a critical subunit of the 70-pS K channel, accounting for the loss of apical K secretory channel activity in ROMK Bartter syndrome.
机译：顶端钾的再循环对于通过厚的上升肢体（TAL）进行盐运输至关重要。 K通道ROMK（Kir1.1; KCNJ1）中的功能丧失突变引起Bartter综合征，这是一种遗传异质性疾病，其特征是TAL的盐吸收严重降低，Na浪费，多尿和低钾性碱中毒。 ROMK（-/-）null小鼠表现出Bartter表型，并且在TAL中缺少小电导（30-pS）顶端K通道（SK）。但是，独特的70-pS K通道也可以显着促进TAL的顶端传导。现在我们检查ROMK缺失对TAL中70-pS K通道功能表达的影响。 70-pS K通道的功能性表达在对照K日粮的ROMK（+ / +）小鼠中较低[平均通道活性（NP（o））= 0.02]，但在2周内通过高K摄入而增加至0.27。相反，高钾饮食可使SK的NP（o）降低约30％，从2.04降至1.44。在对照K日粮上的ROMK杂合（+/-）小鼠中，SK活性约为在ROMK（+ / +）小鼠中观察到的SK活性的一半（0.95对2.04）。高K饮食还可以使ROMK（+/-）小鼠的SK活性降低约40％（从0.95到0.55），但将ROMK（+/-）中70-pS K通道的NP（o）从0增加到0.09 ） 老鼠。这相当于在ROMK（+ / +）小鼠中观察到的通道活性的大约30％（NP（o）= 0.27）。在正常或高K饮食下，在ROMK（-/-）小鼠的TAL细胞中均未观察到70-pS和30-pS K通道。因此，通过增加饮食中的K来增强70-pS K通道的功能表达，并需要ROMK的表达。 ROMK可能形成了70 pS K通道的关键亚基，这解释了ROMK Bartter综合征中顶端K分泌通道活性的丧失。

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