Role of the Cytoskeleton in Regulation of Gastric HCl Secretion a
Role of the Cytoskeleton in Regulation of Gastric HCl Secretion a
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细胞骨架在胃 HCl 分泌调节中的作用
DOI：
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发表时间：
1989
影响因子：
5.2
通讯作者：
D. Malinowska
中科院分区：
文献类型：
--
作者：
J. Cuppoletti;D. Malinowska
一个多功能和多组分的转运系统负责横跨胃壁细胞顶膜的HC1的atp依赖性分泌。胃质子泵的组成部分包括（H+ + K+） atp酶以及K+和c1进入管腔的净转运机制K+伴随着CI-的等价物，通过顶膜沿电化学梯度离开细胞，然后通过（H+ + K+） atp酶进行K+/H+交换。最终结果是HC1分泌到管腔中，K+在细胞质室和管腔室之间循环。因此，HC1的分泌取决于（H+ + K+） atp酶的存在，以及在同一膜和活跃的f ~ r m中K+和cl转运机制的存在。~ ?~ (H+ + K+) atp酶的功能形式已经被分离出来，并确定了初级序列，但对K+和C1-的转运知之甚少。由K+和C1-驱动的生物离子扩散电位的测量，同位素交换，由这些离子的电化学梯度驱动的K+或C1的6J扩散，6。s和最近膜片钳研究的初步结果表明，K+和c1的转运是通过通道进行的。重金属和二价阳离子抑制H+在胃囊泡中的转运，但作用部位尚不清楚。Ba2+和TEA+抑制K+通道，I2羧酸抑制c1通道，13J4，所有这些药物都抑制HC1的积累。由于电耦合的考虑，抑制任何一个通道都会导致净K+和c1输运的损失，但输运函数可以单独测量和抑制。目前尚不清楚K+和Cltransport功能是位于单个蛋白质上还是单独的蛋白质上。胃壁细胞分泌HC1受到组胺、胃泌素和胆碱能激动剂的刺激。在分泌胃和非分泌胃制备的囊泡中，在电离层尼日利亚菌素存在的情况下测量的总（Hf + K+） atp酶活性是相似的然而，来自分泌胃和非分泌胃的封闭囊泡中的H+积累和（H+ + K+） atp酶活性有很大不同，这反映了它们来自的胃的H+运输特性，K+和c1在这些囊泡中的运输也不同。K+和c1转运发生在分泌胃的囊泡中，而在非分泌胃的囊泡中则不活跃。因此，HC1分泌的调节似乎涉及K+和/或c1通道的调节，因为如果通过预加载K+盐，通过使用离子载体如尼古菌素，或使用K+的渗透类似物，ammo-绕过KCI途径，（H+ + K+） atp酶的特定活性在静止和受刺激囊泡中是相等的
A multifunctional and multicomponent transport system is responsible for the ATP-dependent secretion of HC1 across the apical membrane of the gastric parietal cell. The components of the gastric proton pump include the (H+ + K+) ATPase and mechanisms for the net transport of K+ and C1into the lumen.14 K+ exits the cell through the apical membrane, down its electrochemical gradient, accompanied by equivalents of CI-, and is then available for K+/H+ exchange by the (H+ + K+)ATPase. The net result is secretion of HC1 into the lumen, with K+ recycling between the cytosolic and the luminal compartments. HC1 secretion thus depends on the presence of both the (H+ + K+)ATPase and the K + and Cltransport mechanisms in the same membrane and in an active f ~ r m . ~ ? ~ The (H+ + K+)ATPase has been and isolated in functional forrn,’s6 and the primary sequence determined,7 but much less is known of the transport of K+ and C1-. Measurements of biionic diffusion potential6 driven by K+ and C1-, isotope exchange,6J’ diffusion of K+ or C1driven by electrochemical gradients of these ions,6.s and recent preliminary results of patch clamp studies9J0 suggest that K+ and C1transport occurs through channels. Heavy metals and divalent cations inhibit H+ transport in gastric vesicles,8.11 but the site of action is not known. Ba2+ and TEA+ inhibit the K+ channel,I2 carboxylic acids inhibit the C1channel,13J4 and all of these agents inhibit HC1 accumulation. Inhibition of either channel results in loss of net K+ and C1transport due to electrical coupling considerations, but the transport functions can be measured and inhibited separately. It is not known if the K+ and Cltransport function resides on a single protein or on separate proteins. HC1 secretion by the gastric parietal cell is stimulated by histamine, gastrin, and carbachol (a cholinergic agonist). The total (Hf + K+)ATPase activity as measured in the presence of the ionophore nigericin in vesicles prepared from secreting and nonsecreting stomachs is similar.6 However, H+ accumulation and (H+ + K+)ATPase activity in sealed vesicles from secreting and nonsecreting stomachs are vastly different, reflecting the H + transport properties of the stomach from which they were K+ and C1transport is also different in these vesicles. K + and C1transport occurs across vesicles from secreting stomachs and is inactive across vesicles from nonsecreting Regulation of HC1 secretion thus appears to involve regulation of the K+ and/or C1channels, because the specific activity of the (H+ + K+)ATPase is equal in both resting and stimulated vesicles if the KCI pathway is bypassed by preloading with K + salts, by using ionophores such as nigericin, or using the permeant analog of K+, ammo-
微丝破坏剂对仔猪胃泌酸细胞HCl分泌和超微结构的影响
影响因子：
29.4
作者：
Black,JA;Forte,TM;Forte,JG
通讯作者：
Forte,JG
大鼠胃 (HK )-ATP 酶的分子克隆。
DOI：
--
发表时间：
1986
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Shull,GE;Lingrel,JB
通讯作者：
Lingrel,JB