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Inhibition of K+ conductance in descending vasa recta pericytes by ANG II.

机译:ANG II对降脉络膜直肠周细胞中K +电导的抑制作用。

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摘要

We tested whether K(+) channel inhibition accompanies ANG II-induced depolarization of descending vasa recta (DVR) pericytes. An increase in extracellular K(+) concentration ([K(+)](o)) from 5 to 100 mM depolarized resting pericytes but had no effect after prolonged (10 nM, 20 min) ANG II exposure. In contrast, reduction of extracellular Cl(-) concentration ([Cl(-)](o)) from 154 to 34 mM had a minor effect on resting membrane potential but strongly depolarized pericytes treated with ANG II. The K(+) channel blockers BaCl(2) (0.1, 1 mM) and tetraethylammonium (TEA; 30 mM) depolarized resting pericytes but did not affect membrane potential of ANG II-treated pericytes. Pericyte whole cell currents were reduced by ANG II and nearly eliminated by combined ANG II exposure and the Cl(-) channel blocker niflumic acid (100 muM). Augmentation of inward current induced by raising [K(+)](O) from 5 to 50 mM was eliminated by preexposure to ANG II. TEA- and BaCl(2)-sensitive outward currents, generated by depolarizing pericytes from -80 to -40 mV, were eliminated by ANG II. We conclude that ANG II depolarizes DVR pericytes by a combination of Cl(-) channel activation and K(+) channel inhibition.
机译:我们测试了K(+)通道抑制是否伴随ANG II诱导的降脉管直肠(DVR)周细胞去极化。胞外K(+)浓度([K(+)](o))从5 mM增至100 mM去极化静息周细胞,但长时间(10 nM,20分钟)ANG II暴露后无作用。相比之下,将细胞外Cl(-)浓度([Cl(-)](o))从154降低至34 mM对静息膜电位的影响较小,但用ANG II处理的细胞则强烈去极化。 K(+)通道阻滞剂BaCl(2)(0.1,1 mM)和四乙铵(TEA; 30 mM)使静止的周细胞去极化,但不影响ANG II处理的周细胞的膜电位。 ANG II降低了周细胞全细胞电流,并且通过ANG II暴露和Cl(-)通道阻滞剂尼氟酸(100μM)的结合几乎消除了周细胞全细胞电流。通过将[K(+)](O)从5 mM提高到50 mM引起的内向电流的增加通过预先暴露于ANG II而消除。 ANG II消除了对周细胞从-80到-40 mV去极化而产生的TEA和BaCl(2)敏感的向外电流。我们得出结论,ANG II通过Cl(-)通道激活和K(+)通道抑制相结合使DVR周细胞去极化。

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