Chapter 23
The Digestive System
871
23
As H
1
is pumped from the cell and HCO
3
2
(bicarbonate ion)
accumulates within the cell, HCO
3
2
is ejected through the baso-
lateral cell membrane into the capillary blood. As a result, blood
draining from the stomach is more alkaline than the blood serv-
ing it. Tis phenomenon is called the
alkaline tide
. Notice that
a HCO
3
2
-Cl
2
antiporter in the basolateral membrane moves
HCO
3
2
and Cl
2
in opposite directions, and this is how the Cl
2
moves into the lumen as the chloride part of the HCl product.
K
1
and Cl
2
move into the stomach lumen by diffusing through
membrane channels.
Phase 3: Intestinal
Te
intestinal phase
of gastric secretion has two components—
stimulatory and inhibitory (see Figure 23.17). Te excitatory
aspect is set into motion as partially digested food fills the
initial part (duodenum) of the small intestine. Tis stimulates
cells, are used to treat gastric ulcers due to hyperacidity. So, as
you might guess, histamine is the major player here.
HCl Formation
Te process of HCl formation within the pari-
etal cells is complicated, but it appears to go something like this
(Figure 23.18)
: When parietal cells are appropriately stimu-
lated, H
1
is actively pumped into the stomach lumen against a
tremendous concentration gradient by H
1
-K
1
A±Pases in ex-
change for K
1
ions that move into the cell. K
1
then cycles back
into the lumen via K
1
channels. Chloride ions (Cl
2
) follow H
1
into the lumen to maintain an electrical balance in the stomach,
completing the process of HCl secretion. Te Cl
2
is obtained
from blood plasma, while H
1
comes from the breakdown of
carbonic acid (formed by the combination of carbon dioxide
and water) within the parietal cell:
CO
2
1
H
2
O
S
H
2
CO
3
S
H
1
1
HCO
3
2
Sight and thought
of food
Stomach
distension
activates
stretch
receptors
Presence of
partially digested
foods in duodenum
or distension of the
duodenum when
stomach begins to
empty
Stimulation of
taste and smell
receptors
Food chemicals
(especially peptides and
caffeine) and rising pH
activate chemoreceptors
Loss of
appetite,
depression
1
Excessive
acidity
(pH < 2)
in stomach
Distension
of duodenum;
presence of
fatty, acidic, or
hypertonic
chyme; and/or
irritants in
the duodenum
Emotional
stress
Distension;
presence of
fatty, acidic,
partially
digested food
in the
duodenum
Stimulatory events
Inhibitory events
Cephalic
phase
Gastric
phase
Intestinal
phase
Lack of
stimulatory
impulses to
parasym-
pathetic
center
Cerebral
cortex
Cerebral cortex
Conditioned reflex
Brief
effect
Vagovagal
reflexes
Local
reflexes
Medulla
G cells
Hypothalamus
and medulla
oblongata
Vagus
nerve
Vagus
nerve
Intestinal
(enteric)
gastrin
release
to blood
Gastrin
release
to blood
Stomach
secretory
activity
Gastrin
secretion
declines
G cells
Overrides
parasym-
pathetic
controls
Sympathetic
nervous
system
activation
Entero-
gastric
reflex
Release of
enterogastrones
(secretin, cholecystokinin,
vasoactive intestinal
peptide)
Local
reflexes
Vagal
nuclei
in medulla
Pyloric
sphincter
Stimulate
Inhibit
1
1
1
1
1
1
2
2
2
2
Figure 23.17
Neural and hormonal mechanisms that regulate release of gastric juice.
Stimulatory factors are shown on the left; inhibitory factors are shown on the right.
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