Physiology of Gastric Acid Secretion

The secretion of gastric acid is the principle role of the gastric oxyntic gland apparatus and is regulated by a complex neurohormonal process. Interplay between neurocrine, paracrine, and endocrine regulation occurs via acetylcholine, histamine, and gastrin, respectively for each of these processes. The parietal cell is primarily responsible for the synthesis and release of acid; however other cellular components of the oxyntic gland include the gastric D cells and enterchromaffin-like (ECL) cells. In general, acid secretion can be divided into the following two phases: (1) the cephalic phase and (2) the peripheral phase (Zeng et al, 1999).

The major neural regulator of acid secretion is through the vagus nerve. Stimulation by the vagus nerve results in cholinergic stimulation of the muscarinic receptor on the parietal cell (Wolfe and Soll, 1988). Our understanding of the mechanisms involved in the cephalic phase of acid secretion have been improved by the observation that enteric neurons in the gastric mucosa contain the neu-ropeptide, pituitary adenylate cyclase activating polypep-tide (PACAP) which has been shown to stimulate release of histamine from the ECL cell (Zeng et al, 1999). Presumably, higher cortical perceptions of food activate the cephalic phase of acid secretion.

The peripheral phase of gastric acid secretion occurs once food comes into contact with the gastric mucosa. Ingested proteins stimulate the release of gastrin from gastric G cells. The receptor-mediated pathway for this process is still largely unknown. Gastrin released from the G cell stimulates the CCK-2 or gastrin receptor that is expressed on the gastric ECL cell. Gastrin, like PACAP, stimulates the release of histamine from the ECL cell. Histamine acts at the histamine-2 (H2) receptor expressed on the parietal cell to stimulate hydrogen/potassium ATPase (H+/K+-ATPase).

Constipation Prescription

Constipation Prescription

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