Gastric Phase

The arrival of food into the stomach stimulates the gastric phase of regulation. Gastric secretion is stimulated in response to two factors: (1) distension of the stomach, which is determined by the amount of chyme, and (2) the chemical nature of the chyme.

While intact proteins in the chyme have little stimulatory effect, the partial digestion of proteins into shorter polypeptides and amino acids, particularly phenylalanine and tryptophan, stimulates the chief cells to secrete pepsinogen and the G cells to secrete gas-trin. Gastrin, in turn, stimulates the secretion of pepsinogen from chief cells, but its effect on the parietal cells is primarily indirect. Gastrin stimulates the secretion of histamine from ECL cells, and the histamine then stimulates secretion of HCl from parietal cells, as previously described (fig. 18.30). A positive feedback mechanism thus develops. As more HCl and pepsinogen are secreted, more short polypeptides and amino acids are released from the ingested protein. This stimulates additional secretion of gastrin and, therefore, additional secretion of HCl and pepsinogen. It should be noted that glucose in the chyme has no effect on gastric secretion, and the presence of fat actually inhibits acid secretion.

■ Figure 18.30 The regulation of gastric acid secretion. The presence of amino acids in the stomach lumen from partially digested proteins stimulates gastrin secretion. Gastrin secretion from G cells is also stimulated by vagus nerve activity. The secreted gastrin then acts as a hormone to stimulate histamine release from the ECL cells. The histamine, in turn, acts as a paracrine regulator to stimulate the parietal cells to secrete HCl. (© = stimulation; Q = inhibition.)

Secretion of HCl during the gastric phase is also regulated by a negative feedback mechanism. As the pH of gastric juice drops, so does the secretion of gastrin—at a pH of 2.5, gastrin secretion is reduced, and at a pH of 1.0 gastrin secretion ceases. The secretion of HCl thus declines accordingly. This effect may be mediated by the hormone somatostatin, secreted by the D cells of the gastric mucosa. As the pH of gastric juice falls, the D cells are stimulated to secrete somatostatin, which then acts as a paracrine regulator to inhibit the secretion of gastrin from the G cells.

The presence of proteins and polypeptides in the stomach helps to buffer the acid and thus to prevent a rapid fall in gastric pH. More acid can thus be secreted when proteins are present than when they are absent. The arrival of protein into the stomach thus stimulates acid secretion in two ways—by the positive feedback mechanism previously discussed and by inhibition of the negative feedback control of acid secretion. Through these mechanisms, the amount of acid secreted is closely matched to the amount of protein ingested. As the stomach is emptied the protein buffers exit, the pH thus falls, and the secretion of gas-trin and HCl is accordingly inhibited.

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