Secretory modulation of basolateral membrane inwardly rectified K(+) channel in guinea pig distal colonic crypts.

Secretory modulation of basolateral membrane inwardly rectified K(+) channel in guinea pig distal colonic crypts.
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豚鼠远端结肠隐窝基底外侧膜向内整流 K( ) 通道的分泌调节。

DOI:
10.1152/ajpcell.00065.2001
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发表时间:
2002
期刊:
American journal of physiology. Cell physiology
影响因子:
--
通讯作者:
Halm,DanR
Halm,DanR
中科院分区:
--
文献类型:
--
作者:
Li,Yingjun;Halm,DanR

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细胞贴附记录显示豚鼠远端结肠隐窝基底外侧膜的K+通道活性。使用含有140 mM K+的移液器溶液时,抑制整流电流明显。在静息膜电位下,单通道电导(γ)为9 pS。偶见γ = 19 pS的内向整流器。在保持电位为−80 mV时,γ分别为21和41 pS。通过改变浴离子组成,在贴片切除后确认K+通道的身份。从反转电位来看,Na+对K+的相对渗透性(PNa/PK)为0.02 ± 0.02,其中PRb/PK= 1.1,PCl/PK< 0.03。自发开放概率(Po)的9-pS内向整流(gpKir)是电压独立的细胞贴附补丁。观察到低(Po= 0.09 ± 0.01)和中等(Po= 0.41 ± 0.01)活动模式。切离使dgpKir向中等活性模式移动,PoofgpKir不受电解液Ca ~(2+)活性和电解液酸化的影响。添加Cl−和K+促分泌素改变了PoofgpKir。毛喉素或卡巴胆碱(10 μM)激活小电导率的Kirin静止斑,增加低活动斑的Poin。K+促分泌素,肾上腺素(5 μM)或前列腺素E2(100 nM),减少PoofgpKirin活性斑块。ThisgpKir可能参与跨结肠上皮的Cl−和K+的产电分泌,这需要在最大Cl−分泌期间有较大的基底外侧膜K+电导,并且推测在初级产电K+分泌期间有较低的K+电导。
Cell-attached recordings revealed K+channel activity in basolateral membranes of guinea pig distal colonic crypts. Inwardly rectified currents were apparent with a pipette solution containing 140 mM K+. Single-channel conductance (γ) was 9 pS at the resting membrane potential. Another inward rectifier with γ of 19 pS was observed occasionally. At a holding potential of −80 mV, γ was 21 and 41 pS, respectively. Identity as K+channels was confirmed after patch excision by changing the bath ion composition. From reversal potentials, relative permeability of Na+over K+(PNa/PK) was 0.02 ± 0.02, withPRb/PK= 1.1 andPCl/PK< 0.03. Spontaneous open probability (Po) of the 9-pS inward rectifier (gpKir) was voltage independent in cell-attached patches. Both a low (Po= 0.09 ± 0.01) and a moderate (Po= 0.41 ± 0.01) activity mode were observed. Excision movedgpKirto the medium activity mode;PoofgpKirwas independent of bath Ca2+activity and bath acidification. Addition of Cl−and K+secretagogues alteredPoofgpKir. Forskolin or carbachol (10 μM) activated the small-conductancegpKirin quiescent patches and increasedPoin low-activity patches. K+secretagogues, either epinephrine (5 μM) or prostaglandin E2(100 nM), decreasedPoofgpKirin active patches. ThisgpKirmay be involved in electrogenic secretion of Cl−and K+across the colonic epithelium, which requires a large basolateral membrane K+conductance during maximal Cl−secretion and, presumably, a lower K+conductance during primary electrogenic K+secretion.
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