Hydrogen potassium ATPase

The gene ATP4A[4] encodes the H+/K+ ATPase α subunit, and is a ~1000-amino acid protein that contains the catalytic sites of the enzyme and forms the pore through the cell membrane that allows the transport of ions.

The structure of H+/K+ ATPase has been determined for humans, dogs, hogs, rats, and rabbits and is 98% homologous across all species.

[citation needed] The hydrogen potassium ATPase is activated indirectly by gastrin that causes ECL cells to release histamine.

[13] Reducing acidity alleviates disease symptoms but does not treat the actual cause of GERD (abnormal relaxation of the esophageal sphincter) or PUD (Helicobacter pylori and NSAIDs).

This type of inhibitor is effective in treating ulcers but does not prevent them from forming, and patients develop tolerance to them after about one week, leading to a 50% reduction in efficacy.

The use of PPIs has not been correlated with an elevated risk of anemia, so the H+/K+-ATPase is thought to aid iron absorption but is not necessarily required.

[18] Current association of dementia and PPIs have been documented in Germany and in research articles denoting how Benzimidazole derivatives, Astemizole (AST) and Lansoprazole (LNS) interact with anomalous aggregates of tau protein (neurofibrillary tangles).

[19][20][21] Current theories include the non-selective blockade of sodium-potassium pumps in the brain causing osmotic imbalances or swelling in the cells.

[auth opinion] Interaction of PPIs with other drug affecting the sodium-potassium pump, e.g., digoxin, warfarin etc., has been well documented.

[22] Memory has been associated with astrocytes and the alpha3 subunit of adenosine receptor found in hydrogen/Sodium-potassium pumps may be a focal point in dementia.