550
Chapter 15
The initiation of these refl exes depends upon the con-
tents of both the stomach and small intestine. All the factors
previously discussed that regulate acid secretion (see Table
15–5) can also alter gastric motility. For example, gastrin, in
suffi ciently high concentrations, increases the force of antral
smooth muscle contractions. Distension of the stomach also
increases the force of antral contractions through long and
short refl exes triggered by mechanoreceptors in the stomach
wall. Therefore, after a large meal, the force of initial stomach
contractions is greater, which results in a greater emptying per
contraction.
In contrast, gastric emptying is inhibited by distension
of the duodenum, or the presence of fat, high-acidity (low
pH), or hypertonic solutions in the lumen of the duodenum
(
Figure 15–24
). These are the same factors that inhibit acid
and pepsin secretion in the stomach. Fat is the most potent
of these chemical stimuli. This prevents overfi
lling of the
duodenum.
Autonomic nerve fi bers to the stomach can be activated
by the CNS independently of the refl
exes originating in the
stomach and duodenum and can infl uence gastric motility. An
increase in parasympathetic activity increases gastric motility,
whereas an increase in sympathetic activity decreases motil-
ity. Via these pathways, pain and emotions can alter motil-
ity; however, different people show different gastrointestinal
responses to apparently similar emotional states.
As we have seen, a hypertonic solution in the duode-
num is one of the stimuli inhibiting gastric emptying. This
refl ex prevents the fl uid in the duodenum from becoming too
hypertonic. It does so by slowing the rate of entry of chyme
and thereby the delivery of large molecules that can rapidly
be broken down into many small molecules by enzymes in the
small intestine. A patient whose stomach has been removed
because of disease (e.g., cancer) must eat a number of small
meals. A large meal, in the absence of the controlled emptying
by the stomach, could rapidly enter the intestine, producing
a hypertonic solution. This hypertonic solution could cause
enough water to fl
ow (by osmosis) into the intestine from
Esophagus
Lower
esophageal
sphincter
Duodenum
Pyloric
sphincter
Stomach
Peristaltic
wave
Figure 15–22
Peristaltic waves passing over the stomach force a small amount
of luminal material into the duodenum. Black arrows indicate
movement of luminal material; purple arrows indicate movement of
the peristaltic wave in the stomach wall.
Figure 15–23
Slow wave oscillations in the membrane potential of gastric smooth
muscle fi bers trigger bursts of action potentials when threshold
potential is reached at the wave peak. Membrane depolarization
brings the slow wave closer to threshold, increasing the action
potential frequency and thus the force of smooth muscle contraction.
Action
potentials
Slow waves
Membrane depolarization
Time
Threshold
potential
–60
S
mooth mu
s
cle ten
s
ion
Membrane potential (mV)
0
Time
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