Interplay of potassium channel, gastric parietal cell and proton pump in gastrointestinal physiology, pathology and pharmacology

Formation and Detection of Gizzerosine in Animal Feed Matrices: Progress and Perspectives

“…37,38 (C) E1 conformation due to ATP dephosphorylation binds hydronium ions (E1-P form) from the cytoplasm of the parietal cells, and conformational changes (E2-P form) occur at the same time, so that H + −K + -ATPase releases H3O + into the lumen and binds to K + from outside the cytoplasm, resulting in catalytic subunit dephosphorylation back to E1 conformation. 36,38 K + is released from the ion-binding site into the cytoplasm of parietal cells after ATP binding. supplementation of gizzerosine was different with death occurring at 300 μg/100 g, 100 μg/100 g, and 2 ppm, respectively.…”

“…The hydrolysis of ATP changes the gastric H + –K + -ATPase conformationally through phosphorylation and dephosphorylation, , promoting the outflow of H3O + from parietal cells and the inflow of extracytoplasmic K + . Thus, H + secreted into the gastric lumen combines with Cl – to form gastric acid , (Figure ). The H2 receptor-activated cAMP production is the key and rate-limiting trigger of parietal acid secretion during this process.…”

“…(A) Cellular anatomy of the stomach. (B) Histamine secreted by ECL cells in the corpus binds to H2 receptors on parietal cells, and stimulates AC generating cAMP, activating PKA and inducing the conformational change of H + –K + -ATPase through phosphorylation and dephosphorylation through Gs signal, − which leads to the transfer of H3O + from parietal cells and the inflow of K + from extracellular cells, and the H + secreted into lumen combining with the Cl – in lumen to form gastric acid. , (C) E1 conformation due to ATP dephosphorylation binds hydronium ions (E1-P form) from the cytoplasm of the parietal cells, and conformational changes (E2-P form) occur at the same time, so that H + –K + -ATPase releases H3O + into the lumen and binds to K + from outside the cytoplasm, resulting in catalytic subunit dephosphorylation back to E1 conformation. , K + is released from the ion-binding site into the cytoplasm of parietal cells after ATP binding …”