 This video will cover the following objective from digestive physiology, describe the secretions produced by gastric pits, describe the functions of the autonomic nervous system, and the hormones gastrin, secretin, and CCK in the regulation of the stomach. The stomach receives a bolus from the esophagus and then the bolus is mixed with gastric juice in the mechanical digestion mechanism of churning within the stomach when the muscularis of the stomach wall contracts. The gastric juice has a low pH which helps to denature proteins and also activates the enzyme pepsin which is secreted from gastric pits as an inactive precursor known as pepsinogen. Gastric pits are folds in the surface of the mucosa. The gastric pits contain chief cells that produce the precursor to the enzyme pepsin known as pepsinogen. Pyridose cells found in the gastric pits produce hydrochloric acid These parietal cells also produce intrinsic factor, which is important for the absorption of vitamin B12. As pepsinogen released by chief cells travels out of the gastric pit, it becomes activated by the hydrochloric acid produced by the parietal cells. Gastric juice secretion is stimulated in the cephalic phase by an extrinsic control mechanism where the site or thought of food or the taste or smell of food is processed by the brain and stimulates the control centers in the hypothalamus and medulla oblongata that activate the parasympathetic efferent fibers traveling through the vegas nerve which stimulate the release of acetylcholine in the stomach to stimulate the gastric pits to increase the secretion of gastric juice. In contrast, loss of appetite or depression can lead to decreased parasympathetic activity and increased sympathetic activity inhibiting gastric juice secretion. As food enters the stomach, the chemoreceptors of the enteric nervous system detect nutrients released from the chemical digestion of protein and this will stimulate the production of gastrin from the enteroendocrine G cells of the gastric pits and then gastrin will stimulate the production of gastric juice as an intrinsic control mechanism in the gastric phase of gastric secretions. The gastric phase of gastric secretion is an intrinsic control mechanism when food enters the stomach, the distension of the stomach is stretching of the stomach in response to food, which is detected by stretch receptors, mechanoreceptors of the enteric nervous system. These mechanoreceptors can stimulate a local reflex that activates the secretion of gastric juice. Chemoreceptors detect chemicals from food as well as the increasing pH of the gastric juice as a result of diluting of gastric juice when food enters the stomach. These chemoreceptors will stimulate G cells, the enteroendocrine cells in the gastric pits that produce gastrin. Then gastrin is released into the blood, but has an action locally within the stomach to further increase gastric juice secretion, while the intrinsic mechanism of the gastric phase primarily stimulates an increased gastric secretion and increased churning. Excessive acidity or emotional distress can also lead to decreased gastric secretion and decreased churning. The intestinal phase regulating gastric secretions involves an initial positive feedback mechanism followed by a negative feedback mechanism. Initially, as shown with the orange arrow, the presence of a low pH from chyme entering the duodenum, as well as the presence of partially digested foods releasing nutrients that activate chemoreceptors in the duodenum leads to activation of the enteroendocrine G cells in the small intestine that release intestinal gastrin. Then intestinal gastrin travels in the blood to the stomach where it binds to the receptors in the gastric pits to stimulate increased gastric juice secretion. However, a negative feedback mechanism takes over when the duodenum fills with chyme, the mechanoreceptors detect stretching of that chyme and chemoreceptors detect the release of nutrients and this will lead to activation of the enteroendocrine cells that produce secretin and CCK. Secretin and CCK will then travel through the blood and bind to receptors in the stomach where they have the effect of inhibiting the secretion of gastric juice. The afferent fibers also relay information from these sensory receptors of the enteric nervous system into the central nervous system, which stimulates a enterogastric reflux, which leads to inhibition of the parasympathetic efferent fibers that stimulate gastric secretion leading to decreased gastric secretion as a negative feedback mechanism and this negative feedback mechanism helps to control the volume of chyme exiting the stomach and entering into the duodenum. As a small amount of chyme first enters, it promotes an increase in gastric secretion to promote further movement of chyme into the duodenum until the duodenum becomes filled with chyme at which point the negative feedback mechanisms involving secretin, CCK and the autonomic nervous system have the negative feedback effect of decreasing gastric juice secretion. During the intestinal phase of gastric secretion the presence of acidic chyme entering into the duodenum initially will stimulate the production of intestinal gastrin from the enteroendocrine G cells in the duodenum, which leads to stimulation of increased gastric juice secretion. However, when the small intestine starts to fill with chyme, mechanoreceptors detect stretching of the duodenum and stimulate the enteroendocrine I cells that produce CCK and the enteroendocrine S cells that produce secretin, then CCK and secretin will have the negative feedback effect of decreasing the gastric juice secretion.