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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
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