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Regulation of secretion of gastric acid

Parietal cells are in either resting state
or in a stimulated state but when and how the cells are stimulated? Parietal cells
have receptors for acetylcholine known as muscarinic receptors which are of M3
type. Then there are receptors for gastrin that is released from G cells
from pyloric glands. Also there are receptors for histamine which are of
H2 type. So all these 3: acetylcholine gastrin, histamine can stimulate
parietal cell and can cause increase in HCl secretion but not only that they
also affect release of each other. We can actually simplify it as levels of
control of acid secretion. These levels can be arranged as neural, hormonal and
paracrine manner. So vagus is the one which releases acetylcholine acts in a
neural manner, gastrin is released in blood and acts in hormonal manner. ECL
cells release histamine and which acts on parietal cells in paracrine manner. The
machinery appears little complex but if you think in terms of levels of control
you will get a sense of it. At the top is vagal control which
stimulates acid secretion by directly stimulating parietal cells as we saw
that there are acetylcholine receptors M3 receptors. Then it also causes release
of gastrin from G cells. Not only that it also stimulates theseEterochromaffin like cells which release histamine. Now these cells release somatostatin which
have a inhibitory effect on these. So the effect of vagua is to stimulate HCl
secretion, Vagus actually inhibits these D-cells.
Gastrin forms a second level and when gastrin is released. It stimulates
again the lower levels that is the ECL and also the parietal cells but
again it will have an inhibitory effect on D cells. Then ECL cells which
release histamine acting in a paracrine manner that also stimulates parietal
cells and inhibits T cells releasing somatostatin which is
having negative effect. So if you see in terms of level, the topmost level is
stimulating all three lower levels second level is gastrin:
stimulating the lower two levels and the lowest level
histamine is stimulating parietal cells=with all inhibiting the D cells. But
these are all stimulatory effects for release of HCl. So there should be a
negative control also on the secretion. The secreted acid itself that is the H+
ions have a negative influence of parietal cells since they stimulate
D cells causing release of somatostatin. This somatostatin inhibits
parietal cell, ECL cells and G cells and decreases their secretion thus
decreasing H+ ions. So here is a negative feedback going on to control the level
of hydrogen ions. So this is how machinery is arranged. But when are these
stimulants activated? Now neural stimulation via vagus occurs when you
see, smell or think of food. This is known as cephalic phase of HCl secretion. So
the thought process itself will stimulate HCl secretion. When food
enters into stomach, local distension of the stomach and peptides in food
stimulate these G cells causing release of gastrin so this is a local effect. This
is known as gastric phase. Now distension of the stomach also activates local
reflexes causing stimulation of the vagus again. But what happens when
partially digested food of stomach that is chyme enters the duodenum. Now depending
on the contents of the chyme. there are secretions in duodenum which
also have effect on HCl secretion. The fat content in chyme causes release of
CCK: cholecystokinin, acidic content causes release of another
hormone secreti,n both of which have inhibitory effect on release of gastrin.
So this effect of intestine on the release of HCl secretion is known as
intestinal phase. Now this phase is also very important because it ensures proper
pH in duodenum and that it does not become too acidic since enzymes there
act in alkaline environment only. So if it becomes too acidic there is a signal
back to the stomach to decrease the HCl secretion. So there are different phases
of acid secretion which act via different mechanisms. There is cephalic
phase which acts on thought, smell of food, there is a gastric phase which
occurs when food enters into the stomach and when food enters into the duodenum
there is intestinal phase.

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