Helander H F
Baillieres Clin Gastroenterol. 1988 Jul;2(3):539-54. doi: 10.1016/s0950-3528(88)80004-6.
The parietal cells possess the unique capacity to produce large quantities of acid at a high concentration, and this is reflected in unique properties at the cellular level. The cells are comparatively large, and they are equipped with secretory canaliculi, a multitude of mitochondria, and cytoplasmic tubulovesicles. During secretion many of the tubulovesicles merge with the secretory canaliculi, which then expand. In the process H+, K+-ATPase is transferred from the tubulovesicular membrane to the secretory membrane. This enzyme catalyses the final step in the production of HCl. Parietal cell activity is regulated through receptors on the basolateral cell surfaces. In the isolated gland and in the isolated parietal-cell fractions, stimulation of receptors for histamine evokes higher secretion than receptor stimulation with cholinergic compounds or with gastrin. In these experimental models, specific inhibitors are required to block acid secretion; for example histamine H2-receptor antagonists will block histamine-induced secretion but will be inactive when secretion is evoked by gastrin or by cholinergic stimulation. These stimuli cause a more or less marked increase in the intracellular levels of Ca2+, which acts as a second messenger, leading to the activation of phosphokinases and, ultimately, to morphological transformation of the parietal cells and acid secretion. Another such intracellular messenger is cAMP, which is formed in response to histamine stimulation only; prostaglandins may prevent this process and block acid secretion. The final step in the production of acid requires K+ and Cl- channels in the secretory membrane and the H+, K+-ATPase-catalysed exchange of K+ for H+ across this membrane. This reaction consumes large amounts of energy and depends on the aerobic production of ATP by the parietal cells. Substituted benzimidazoles, such as omeprazole, accumulate in the acid compartments of the parietal cells and inhibit the H+, K+-ATPase, thereby blocking acid production.
壁细胞具有以高浓度产生大量胃酸的独特能力，这在细胞水平上表现为独特的特性。这些细胞相对较大，配备有分泌小管、大量线粒体和细胞质微管泡。在分泌过程中，许多微管泡与分泌小管融合，然后分泌小管扩张。在此过程中，H⁺，K⁺ -ATP酶从微管泡膜转移至分泌膜。该酶催化盐酸生成的最后一步。壁细胞的活性通过细胞基底外侧表面的受体进行调节。在分离的腺体和分离的壁细胞组分中，组胺受体的刺激比胆碱能化合物或胃泌素刺激受体引起更高的分泌。在这些实验模型中，需要特定的抑制剂来阻断胃酸分泌；例如，组胺H2受体拮抗剂将阻断组胺诱导的分泌，但在胃泌素或胆碱能刺激引起分泌时则无活性。这些刺激或多或少会显著增加细胞内Ca²⁺水平，Ca²⁺作为第二信使，导致磷酸激酶激活，并最终导致壁细胞形态转变和胃酸分泌。另一种这样的细胞内信使是cAMP，它仅在组胺刺激下形成；前列腺素可能会阻止这一过程并阻断胃酸分泌。胃酸生成的最后一步需要分泌膜中的K⁺和Cl⁻通道以及H⁺，K⁺ -ATP酶催化的K⁺与H⁺跨此膜的交换。该反应消耗大量能量，并依赖于壁细胞需氧产生ATP。取代苯并咪唑类，如奥美拉唑，在壁细胞的酸性区室中蓄积并抑制H⁺，K⁺ -ATP酶，从而阻断胃酸生成。
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