The Physiology of Gastric Secretions 4
January 30th 2010 16:31
Regulation of Gastric Secretion by Nervous and Hormonal Mechanism
The basic factors that stimulate gastric secretion are acetylcholine (involved via vagal/parasympathetic stimulation), gastrin, and histamine. These substances function by attaching to specific receptors, leading to the secretion of the gastric glands. Acetylcholine excites all glands involved in the secretion of hydrochloric acid, pepsinogen, and mucus. Histamine and gastrin, on the other hand, strongly stimulate the secretion of hydrochloric acid by the parietal cells but have little effect in stimulating other gastric secretory cells.
The enteric nervous system can stimulate release of H (to form HCl), either directly or indirectly. The nerve endings of fibers innervating the parietal cells secrete acetylcholie at the neuroeffector junction. The corresponding receptor is M3. Succeeding events include the increase in cytosolic calcium, stimulation of protein kinases, and activation of H /K ATPase. The end result is increased hydrochloric acid secretion.
The indirect stimulation of the parietal cells by the nervous system occurs as acetylcholine attaches to M1 receptor of enterochromaffin-like cells. This gives way to the release of histamine. Histamine in turn binds to H2 receptors found in the parietal cells. Afterwards adenylyl cyclase gets activated. This increases intracellular cAMP, activating protein kinase. Eventually this will stmulate H /K ATPase.
The same direct and indirect mechanisms can be onserved in parietal stimulation by gastrin-secreting cells.
The basic factors that stimulate gastric secretion are acetylcholine (involved via vagal/parasympathetic stimulation), gastrin, and histamine. These substances function by attaching to specific receptors, leading to the secretion of the gastric glands. Acetylcholine excites all glands involved in the secretion of hydrochloric acid, pepsinogen, and mucus. Histamine and gastrin, on the other hand, strongly stimulate the secretion of hydrochloric acid by the parietal cells but have little effect in stimulating other gastric secretory cells.
The enteric nervous system can stimulate release of H (to form HCl), either directly or indirectly. The nerve endings of fibers innervating the parietal cells secrete acetylcholie at the neuroeffector junction. The corresponding receptor is M3. Succeeding events include the increase in cytosolic calcium, stimulation of protein kinases, and activation of H /K ATPase. The end result is increased hydrochloric acid secretion.
The indirect stimulation of the parietal cells by the nervous system occurs as acetylcholine attaches to M1 receptor of enterochromaffin-like cells. This gives way to the release of histamine. Histamine in turn binds to H2 receptors found in the parietal cells. Afterwards adenylyl cyclase gets activated. This increases intracellular cAMP, activating protein kinase. Eventually this will stmulate H /K ATPase.
The same direct and indirect mechanisms can be onserved in parietal stimulation by gastrin-secreting cells.
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