Drugs That Decrease Or Neutralize Gastric Acid Secretion

Functionally, the gastric mucosa is divided into three areas of secretion. The cardiac gland area secretes mucus and pepsinogen.The oxyntic (parietal) gland area, which corresponds to the fundus and body of the stomach, secretes hydrogen ions, pepsinogen, and bicarbonate. The pyloric gland area in the antrum secretes gastrin and mucus.

The parietal cells secrete H+ in response to gastrin, cholinergic, and histamine stimulation (Fig. 40.1). Both cholinergic- and gastrin-induced types of stimulation bring about a receptor-mediated rise in intracellular calcium, an activation of intracellular protein kinases, and eventually an increased activity of the H+-K+ pump leading to acid secretion into the gastric lumen. Following histamine stimulation, a guanine nucleotide-binding protein (Gs) activates adenylyl cyclase, leading to an increase in intracellular levels of the second messenger, cyclic adenosine monophosphate (cAMP). Activation of cAMP-dependent protein kinases initiates the stimulation of the H+-K+ pump.

The cephalic-vagal axis, gastric distention, and local mucosal chemical receptors can modulate acid secretion by the stomach. The smell, taste, sight, or discussion of food may result in cephalic-vagal postganglionic cholinergic stimulation of target parietal cells and enhanced antral gastrin release. After food is ingested, gastric distention initiates vagal stimulation and short intragastric neural reflexes, both of which increase acid secretion. Proteins in ingested meals also stimulate acid

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