The Parietal Cells Are Stimulated to Secrete by the Action of Acetylcholine, Gastrin, and Histamine
Gastric acid secretion is stimulated by the anticipation of eating and the presence of undigested food in the stomach. When an animal anticipates eating, parasympathetic vagal impulses stimulate cells of the enteric nervous system (ENS), which in turn release acetylcholine (ACh) into the vicinity of G cells and parietal cells.
These secretory cells have ACh receptors on their surfaces and respond by secreting gastrin and HCl, respectively. Gastrin circulates in the bloodstream and eventually finds its way to the parietal cells, which have gastrin receptors, in addition to ACh receptors, on their surfaces. The combined actions of gastrin and ACh on the parietal cells result in high rates of HCI flow. The response of the stomach to anticipatory stimuli originating in the brain is referred to as the cephalic phase of gastric secretion.Food entering the stomach initiates the second phase, or “gastric phase,” of gastric secretion. Distention of the stomach by food stimulates stretch receptors, providing afferent stimulation of the ENS; the system responds by direct nervous (ACh) stimulation of the G and parietal cells. In addition, food acts as a buffer, raising the stomach pH. This removes the inhibiting effect of acid on G-cell secretion, further stimulating the production of gastrin, which leads to even greater enhancement of acid production by the parietal cells.
Histamine plays a role as an amplifying substance in gastric acid secretion. Parietal cells have surface receptors for gastrin, ACh, and histamine. They are stimulated maximally when all three receptors are occupied. Histamine is secreted by mast cells and enterochromaffin-like cells in the parietal mucosa. The histamine-secreting cells are stimulated to secrete by gastrin and ACh. Thus the effects of gastrin and ACh on gastric acid secretion are amplified through their stimulation of histamine secretion.
As gastric secretion and digestion proceed, the pH of the stomach decreases. When the stomach pH falls to about 2, gastrin secretion is suppressed, and at a pH of 1, gastrin secretion is completely abolished. Thus the gastrin stimulus to the parietal cells is removed, and acid secretion is reduced (see Figure 27-9).
The intestinal environment also influences the secretion of gastric acid. As acid contents from the stomach flow into the duodenum and the duodenal pH is reduced, gastric acid production is suppressed. The exact mechanism by which duodenal acidification exerts negative feedback on the parietal cells is unclear. The hormone secretin, produced in the duodenum, may be involved, as well as neuronal reflexes acting through the ENS.
The secretion of pepsinogen appears to be under the same regulatory influences as the secretion of HCL However, regulation of pepsin secretion has been researched much less than regulation of HCl secretion.