Role of K₂p channels in stimulus-secretion coupling.
Role of K₂p channels in stimulus-secretion coupling.
复制标题
K-p 通道在刺激-分泌耦合中的作用。
DOI：
10.1007/s00424-014-1663-3
复制
发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Kang,Dawon
中科院分区：
文献类型：
--
作者：
Kim,Donghee;Kang,Dawon
双孔结构域K+(K2P)通道因其高度的基础活性和对各种生物刺激的敏感性而参与多种生理过程。其中一个过程是激素和递质的分泌，以响应刺激，如缺氧、酸中毒和受体激动剂。细胞内[Ca~(2+)]([Ca~(2+)]i)的升高是分泌事件的关键，可通过几种机制实现：(A)抑制静息(背景)K~+通道，(B)激活Na~+/Ca~(2+)-通透性通道，(C)从细胞内储存库释放Ca~(2+)。在这里，我们讨论了TASK和TREK在颈动脉小体化学感受器细胞和肾上腺髓质/皮质细胞刺激分泌机制中的作用。研究表明，低氧和酸中毒等刺激通过抑制TASK或Trek而导致细胞去极化和递质/激素分泌。随后开放电压依赖性钙通道产生的[Ca~(2+)]i升高，然后激活一个钠离子通透性阳离子通道，可能有助于维持去极化和[Ca~(2+)]i。血管紧张素II等激动剂可能通过多种机制升高[Ca~(2+)]i，包括抑制TASK/Trek和从内库释放Ca~(2+)，从而导致醛固酮分泌。因此，抑制静息(背景)K+通道和随后激活电压门控钙通道和钠离子非选择性阳离子通道可能是导致激素和递质分泌的常见离子机制。
Two-pore domain K+(K2P) channels are involved in a variety of physiological processes by virtue of their high basal activity and sensitivity to various biological stimuli. One of these processes is secretion of hormones and transmitters in response to stimuli such as hypoxia, acidosis, and receptor agonists. The rise in intracellular [Ca2+] ([Ca2+]i) that is critical for the secretory event can be achieved by several mechanisms: (a) inhibition of resting (background) K+channels, (b) activation of Na+/Ca2+-permeable channels, and (c) release of Ca2+from intracellular stores. Here, we discuss the role of TASK and TREK in stimulus-secretion mechanisms in carotid body chemoreceptor cells and adrenal medullary/cortical cells. Studies show that stimuli such as hypoxia and acidosis cause cell depolarization and transmitter/hormone secretion by inhibition of TASK or TREK. Subsequent elevation of [Ca2+]iproduced by opening of voltage-dependent Ca2+channels then activates a Na+-permeable cation channel, presumably to help sustain the depolarization and [Ca2+]i. Agonists such as angiotensin II may elevate [Ca2+]ivia multiple mechanisms involving both inhibition of TASK/TREK and Ca2+release from internal stores to cause aldosterone secretion. Thus, inhibition of resting (background) K+channels and subsequent activation of voltage-gated Ca2+channels and Na+-permeable non-selective cation channels may be a common ionic mechanism that lead to hormone and transmitter secretion.