VASOPRESSIN INCREASES DENSITY OF APICAL LOW-CONDUCTANCE K+ CHANNELS IN RAT CCD
VASOPRESSIN INCREASES DENSITY OF APICAL LOW-CONDUCTANCE K+ CHANNELS IN RAT CCD
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DOI：
10.1152/ajprenal.1993.264.3.f502
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发表时间：
1993-03-01
影响因子：
--
通讯作者：
WANG, WH
中科院分区：
文献类型：
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作者：
CASSOLA, AC;GIEBISCH, G;WANG, WH
用膜片钳技术研究了精氨酸加压素（AVP）对正常和高钾饮食大鼠皮质集合管（CCD）主细胞顶膜低电导钾通道的影响。AVP刺激在控制和高K+动物的顶端低电导K+通道活性：应用110-220 pM AVP诱导低电导K+通道密度的显着增加。在磷酸二酯酶抑制剂（3-异丁基-1-甲基黄嘌呤）的存在下，22 pM AVP的管理也增加通道活性。通过同时应用毛喉素和3-异丁基-1-甲基黄嘌呤来模拟AVP对低电导K+通道活性的作用。外源性应用N6，2 ′-O-二丁酰腺苷3 ′，5 ′-环一磷酸（二丁酰-cAMP，0.4-0.8 mM）也增加顶端低电导K+通道活性。由于通道开放概率（P（o））在AVP不存在下几乎饱和，所以由AVP、毛喉素和二丁酰-cAMP诱导的通道活性的增加主要是由于刺激先前沉默的K+通道。我们的结论是，AVP诱导增加低电导K+通道活性的主细胞在大鼠CCD的cAMP依赖性蛋白激酶的刺激。AVP诱导的低电导K+通道活性的增加，因此可以显着地有助于在大鼠CCD中的腺苷诱导的K+分泌。
The effect of arginine vasopressin (AVP) on the low-conductance K+ channel in the apical membrane of rat cortical collecting duct (CCD) principal cells from animals on a control and high-K+ diet was studied using patch-clamp techniques. AVP stimulated apical low-conductance K+ channel activity in both control and high-K+ animals: application of 110-220 pM AVP induced a significant increase in the density of low-conductance K+ channels. In the presence of phosphodiesterase inhibitor (3-isobutyl-1-methylxanthine), administration of 22 pM AVP also increased channel activity. The action of AVP on low-conductance K+ channel activity was mimicked by simultaneous application of forskolin and 3-isobutyl-1-methylxanthine. Exogenously applied N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (dibutyryl-cAMP, 0.4-0.8 mM) also increased apical low-conductance K+ channel activity. Since channel open probability (P(o)) was almost saturated in the absence of AVP, the increase of channel activity induced by AVP, forskolin, and dibutyryl-cAMP resulted predominantly from stimulating previously silent K+ channels. We conclude that AVP induces an increase of low-conductance K+ channel activity of principal cells in rat CCD by the stimulation of cAMP-dependent protein kinase. The AVP-induced increase of low-conductance K+ channel activity can thus significantly contribute to the hormone-induced K+ secretion in the rat CCD.