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Neural and Hormonal Integration  of the mucosa. (a) Gastrin and cholecystokinin
                                       (CCK) and (b) secretin and GIP are structurally
       Endocrine and paracrine hormones and neu-  similar; so are glucagon (! p. 282ff.) and VIP.
       rotransmitters control GI motility, secretion,  High concentrations of hormones from the
       perfusion and growth. Reflexes proceed within  same family therefore have very similar ef-
       the mesenteric and submucosal plexus (enteric  fects.
       nervous system, ENS ), and external innervation  Gastrin occurs in short (G17 with 17 amino
       modulates ENS activity.         acids, AA) and long forms (G34 with 34 AA).
         Local reflexes are triggered by stretch sen-  G17 comprises 90% of all antral gastrin. Gastrin
       sors in the walls of the esophagus, stomach  is secreted in the antrum and duodenum. Its
       and gut or by chemosensors in the mucosal  release (! A1) via gastrin-releasing peptide
       epithelium and trigger the contraction or re-  (GRP) is subject to neuronal control; gastrin is
    Nutrition and Digestion  oral (ca. 2 mm) and anal regions (20–30 mm).  ach. Its secretion is inhibited when the pH of
       laxation of neighboring smooth muscle fibers.
                                       also released in response to stomach wall
                                       stretching and protein fragments in the stom-
       Peristaltic reflexes extend further towards the
                                       the gastric/duodenal lumen falls below 3.5
       They are mediated in part by interneurons and
                                       (! A1). The main effects of gastrin are acid
       help to propel the contents of the lumen
                                       secretion and gastric mucosal growth (! A2).
       through the GI tract (peristalsis).
                                        Cholecystokinin, CCK (33 AA) is produced
         External innervation of the GI tract (cf.
       nervous system (from lower esophagus to as-
                                       chain fatty acids, AA and oligopeptides in the
                                       lumen stimulate the release of CCK (! A1). It
       cending colon) and sympathetic nervous sys-
    10  p. 78ff.) comes from the parasympathetic  throughout small intestinal mucosa. Long-
       tem. Innervation is also provided by visceral
                                       causes the gallbladder to contract and inhibits
       afferent fibers (in sympathetic or parasympa-  emptying of the stomach. In the pancreas, it
       thetic nerves) through which the afferent im-  stimulates growth, production of enzymes and
                                                  –
       pulses for supraregional reflexes flow.  secretion of HCO 3 (via secretin, see below)
                                       (! A2).
       ENS function is largely independent of external inner-  Secretin (27 AA) is mainly produced in the
       vation, but external innervation has some advan-
       tages (a) rapid transfer of signals between relatively  duodenum. Its release is stimulated by acidic
       distant parts of the GI tract via the abdominal ganglia  chyme (! A1). Secretin inhibits acid secretion
       (short visceral afferents) or CNS (long visceral affer-  and gastric mucosal growth and stimulates
       ents); (b) GI tract function can be ranked subordinate  HCO 3 secretion (potentiated by CCK), pan-
                                          –
       to overall body function (c) GI tract activity can be  creatic growth and hepatic bile flow (! A2).
       processed by the brain so the body can become  GIP (glucose-dependent insulinotropic pep-
       aware of them (e.g., stomach ache).
                                       tide, 42 AA; formerly called gastric inhibitory
       Neurotransmitters. Norepinephrine (NE) is re-  polypeptide = enterogastrone) is produced in
       leased by the adrenergic postganglionic neu-  the duodenum and jejunum and released via
       rons, and acetylcholine (ACh) is released by  protein, fat and carbohydrate fragments (e.g.,
       pre-  and  postganglionic  (enteric)  fibers  glucose) (! A1). GIP inhibits acid secretion
       (! p. 78ff.). VIP (vasoactive intestinal peptide)  (! A2) and stimulates insulin release (this is
       mediates the relaxation of circular and vascu-  why oral glucose releases more insulin than
       lar muscles of the GI tract. Met- and leu-  intravenous glucose).
       enkephalin intensify contraction of the pyloric,  Motilin (22 AA) is released by neurons in the
       ileocecal and lower esophageal sphincters by  small intestine and regulates interdigestive
       binding to opioid receptors. GRP (gastrin-re-  motility (! A1, 2).
       leasing peptide) mediates the release of  Paracrine transmitters. Histamine, soma-
       gastrin. CGRP (calcitonin gene-related pep-  tostatin and prostaglandin are the main para-
       tide) stimulates the release of somatostatin  crine transmitters in the GI tract.
       (SIH).
         All endocrine hormones effective in the GI
  234
       tract are peptides produced in endocrine cells
       Despopoulos, Color Atlas of Physiology © 2003 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
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