From the FDA Drug Label
Omeprazole belongs to a class of antisecretory compounds, the substituted benzimidazoles, that suppress gastric acid secretion by specific inhibition of the H+/K+ ATPase enzyme system at the secretory surface of the gastric parietal cell Because this enzyme system is regarded as the acid (proton) pump within the gastric mucosa, omeprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production.
The gastric acid secretion physiology involves the H+/K+ ATPase enzyme system at the secretory surface of the gastric parietal cell, which is the acid (proton) pump within the gastric mucosa. This system is responsible for the final step of acid production.
- The inhibition of this enzyme system leads to suppression of gastric acid secretion.
- Omeprazole is a gastric acid-pump inhibitor that blocks the final step of acid production by specific inhibition of the H+/K+ ATPase enzyme system.
- The effect of omeprazole on gastric acid secretion is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus 1.
From the Research
Gastric acid secretion is a complex physiological process regulated by neural, hormonal, and paracrine pathways, with the most recent and highest quality study 2 highlighting the crucial role of gastrin, histamine, and acetylcholine in stimulating acid secretion. The stomach produces approximately 2-3 liters of gastric acid daily, primarily composed of hydrochloric acid (HCl) with a pH between 1 and 3. This secretion occurs through the coordinated activity of specialized cells in the gastric mucosa, including parietal cells, which use the H+/K+ ATPase pump (proton pump) to secrete hydrogen ions into the gastric lumen while taking in potassium ions, as described in 3. The regulation of gastric acid secretion involves three phases:
- Cephalic, triggered by the sight, smell, or thought of food, mediated by vagal stimulation
- Gastric, occurring when food enters the stomach, stretching the walls and releasing gastrin from G cells, which stimulates acid secretion
- Intestinal, involving hormones like secretin and cholecystokinin that can inhibit acid secretion when chyme enters the duodenum Histamine, released by enterochromaffin-like cells, also plays a crucial role by binding to H2 receptors on parietal cells to stimulate acid production, as noted in 4. Understanding this physiology is fundamental for treating conditions like peptic ulcer disease and gastroesophageal reflux disease with medications such as proton pump inhibitors and H2 receptor antagonists, with the most recent study 2 emphasizing the importance of precise regulation of gastric acid secretion to prevent complications. Key stimulants of acid secretion include:
- Gastrin
- Histamine
- Acetylcholine
- Ghrelin While inhibitors include:
- Somatostatin
- Nefstatin-1
- Interleukin-11
- Calcitonin gene-related peptide, as discussed in 5. The recognition of gastrin's role as a trophic hormone has led to new research into its role in carcinogenesis and the development of cholecystokinin-2 receptor antagonists, highlighting the ongoing progress in understanding the regulation of gastric acid secretion in health and disease 2.