Maintenance of the Body
motor impulses via the vagus nerves to parasympathetic enteric
ganglia. Enteric ganglionic neurons then stimulate the stomach
Te enhanced secretory activity that results when we see or
think of food is a
and occurs only when we
like or want the food. If we are depressed or have no appetite,
this part of the cephalic reﬂex is suppressed.
Phase 2: Gastric
Once food reaches the stomach, local neural and hormonal
mechanisms initiate the
(Figure 23.17). Tis
phase lasts three to four hours and provides about two-thirds of
the gastric juice released.
Stimuli and Inhibitors
Te most important stimuli are dis-
tension, peptides, and low acidity. Stomach distension activates
stretch receptors and initiates both local (myenteric) reﬂexes
and long (vagovagal) reﬂexes. In the long type of reﬂex, impulses
travel to the medulla and then back to the stomach via vagal ﬁ-
bers. Both types of reﬂexes lead to acetylcholine (ACh) release,
which in turn stimulates the output of more gastric juice.
Tough neural inﬂuences initiated by stomach distension are
important, the hormone gastrin probably plays a greater role in
stimulating stomach gland secretion during the gastric phase.
Chemical stimuli provided by partially digested proteins, caf-
feine, and rising pH directly activate gastrin-secreting entero-
endocrine cells called
in the stomach antrum. Gastrin
stimulates the release of enzymes, but its main target is the HCl-
secreting parietal cells, which it prods to spew out even more
HCl. Highly acidic (pH below 2) gastric contents
secretion—a situation that commonly occurs between meals.
When protein foods are in the stomach, the pH of the gastric
contents generally rises because proteins act as buﬀers to tie
. Te rise in pH stimulates gastrin secretion and subse-
quently HCl release, which in turn provides the acidic condi-
tions needed to digest proteins. Te more protein in the meal,
the greater the amount of gastrin and HCl released. As proteins
are digested, the gastric contents gradually become more acidic,
which again inhibits the gastrin-secreting cells. Tis negative
feedback mechanism helps maintain optimal pH and working
conditions for gastric enzymes.
Te neural reﬂexes already described also activate G cells.
Stress, fear, anxiety, or anything that triggers the ﬁght-or-ﬂight re-
sponse inhibits gastric secretion because the sympathetic division
overrides parasympathetic controls of digestion (Figure 23.17).
Control of the HCl-secreting parietal cells is multifaceted. It
is stimulated by three chemicals, all of which bind to G protein–
coupled receptors on the parietal cell’s membrane and work
through second-messenger systems.
released by parasympa-
thetic nerve ﬁbers and
secreted by G cells bring about their
eﬀects by increasing intracellular Ca
by the so-called
(ECL) cells mainly in re-
sponse to gastrin, acts through cyclic AMP (cAMP).
When only one of the three chemicals binds to parietal cells,
HCl secretion is scanty, but when all three bind, HCl pours
forth. As we noted earlier, antihistamines, such as cimetidine,
which bind to and block the H
(histamine) receptors of parietal
enzymatic digestion. (Te unfolded amino acid chain is more
accessible to the enzymes.)
Te most important protein-digesting enzyme produced by
the gastric mucosa is pepsin. In infants, however, the stomach
glands also secrete
, an enzyme that acts on milk pro-
tein (casein), converting it to a curdy substance that looks like
soured milk. Additionally, lingual lipase released by the minor
salivary glands may digest some triglycerides in the stomach for
a short time before the lipase itself is digested.
±wo common lipid-soluble substances—alcohol and aspirin—
pass easily through the stomach mucosa into the blood. Alcohol
and aspirin may cause gastric bleeding, so these substances should
be avoided by people with gastric ulcers.
Despite the obvious beneﬁts of preparing food to enter the
intestine, the only stomach function essential to life is secre-
tion of intrinsic factor.
is required for intestinal
absorption of vitamin B
, needed to produce mature erythro-
cytes. In its absence,
results. However, if vi-
is administered by injection, individuals can survive
with minimal digestive problems even a²er total gastrectomy
(p. 885) summarizes the stom-
Since we describe digestion and absorption later, here we will
focus on events that regulate (1) secretory activity of the gastric
glands and (2) stomach motility and emptying.
Regulation of Gastric Secretion
Both neural and hormonal mechanisms control gastric secre-
tion. Under normal conditions the gastric mucosa pours out
as much as 3 L of gastric juice—an acid brew so potent it can
dissolve nails—every day.
Both long (vagus nerve–mediated) and short (local enteric)
nerve reﬂexes provide nervous control (see Figure 23.4, p. 853).
When the vagus nerves stimulate the stomach, secretory activ-
ity of virtually all of its glands increases. (By contrast, activation
of sympathetic nerves depresses secretory activity.) Hormonal
control of gastric secretion is largely the province of gastrin,
which stimulates secretion of enzymes and HCl, and of hor-
mones produced by the small intestine, which are mostly gas-
Stimuli acting at three distinct sites—the head, stomach, and
small intestine—provoke or inhibit gastric secretions. Accord-
ingly, the three phases of gastric secretion are called the
. Te eﬀector site
is the stomach in all cases and, once initiated, one or all three
phases may be occurring at the same time.
Phase 1: Cephalic (Reﬂex)
of gastric secretion occurs
food enters the stomach (Figure 23.17). Only a few min-
utes long, this phase is triggered by the aroma, taste, sight, or
thought of food, and it gets the stomach ready for its upcoming
Sensory inputs from olfactory receptors and taste buds are
relayed to the hypothalamus. Te hypothalamus, in turn, stimu-
lates the vagal nuclei of the medulla oblongata, which transmits