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SECTION V
Gastrointestinal Physiology
mucus secreted by the cells in the necks of the glands. Several
of the glands open on a common chamber
(gastric pit)
that
opens in turn on the surface of the mucosa. Mucus is also se-
creted along with HCO
3
- by mucus cells on the surface of the
epithelium between glands.
The stomach has a very rich blood and lymphatic supply. Its
parasympathetic nerve supply comes from the vagi and its
sympathetic supply from the celiac plexus.
ORIGIN & REGULATION
OF GASTRIC SECRETION
The stomach also adds a significant volume of digestive juices
to the meal. Like salivary secretion, the stomach actually read-
ies itself to receive the meal before it is actually taken in, dur-
ing the so-called cephalic phase that can be influenced by food
preferences. Subsequently, there is a gastric phase of secretion
that is quantitatively the most significant, and finally an intes-
tinal phase once the meal has left the stomach. Each phase is
closely regulated by both local and distant triggers.
The gastric secretions (Table 26–1) arise from glands in the
wall of the stomach that drain into its lumen, and also from
the surface cells that secrete primarily mucus and bicarbonate
to protect the stomach from digesting itself, as well as sub-
stances known as trefoil peptides that stabilize the mucus-
bicarbonate layer. The glandular secretions of the stomach
differ in different regions of the organ. The most characteris-
tic secretions derive from the glands in the fundus or body of
the stomach. These contain two distinctive cell types from
which the gastric secretions arise: the parietal cells, which
secrete hydrochloric acid and intrinsic factor; and the chief
cells, which produce pepsinogens and gastric lipase (Figure
26–5). The acid secreted by parietal cells serves to sterilize the
meal and also to begin the hydrolysis of dietary macromole-
cules. Intrinsic factor is important for the later absorption of
vitamin B
12
, or cobalamin (Figure 26–6). Pepsinogen is the
precursor of pepsin, which initiates protein digestion. Lipase
similarly begins the digestion of dietary fats.
There are three primary stimuli of gastric secretion, each
with a specific role to play in matching the rate of secretion to
functional requirements (Figure 26–7). Gastrin is a hormone
that is released by G cells in the antrum of the stomach both
in response to a specific neurotransmitter released from
enteric nerve endings, known as gastrin releasing peptide
(GRP, or bombesin), and also in response to the presence of
oligopeptides in the gastric lumen. Gastrin is then carried
through the bloodstream to the fundic glands, where it binds
to receptors not only on parietal (and likely, chief cells) to
activate secretion, but also on so-called enterochromaffin-like
cells (ECL cells) that are located in the gland, and release his-
tamine. Histamine is also a trigger of parietal cell secretion,
via binding to H
2
histamine receptors. Finally, parietal and
chief cells can also be stimulated by acetylcholine, released
from enteric nerve endings in the fundus.
During the cephalic phase of gastric secretion, secretion is
predominantly activated by vagal input that originates from the
brain region known as the dorsal vagal complex, which coordi-
nates input from higher centers. Vagal outflow to the stomach
then releases GRP and acetylcholine, thereby initiating secretory
FIGURE 26–3
Regulation of salivary secretion by the parasympathetic nervous system.
ACh, acetylcholine.
(Adapted from Barrett KE:
Gas-
trointestinal Physiology
. McGraw-Hill, 2006.)
Smell
Taste
Sound
Sight
Pressure
in mouth
ACh
ACh
Parasympathetics
Sleep
Fatigue
Increased Fear
salivary
secretion
via effects on
Salivatory
nucleus of
medulla
Higher
centers
Otic
ganglion
- Acinar secretion
- Vasodilatation
Parotid
gland
Submandibular
gland
Submandibular
ganglion
−