Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 26

Overview of Gastrointestinal Function & Regulation 433

function. However, before the meal enters the stomach, there are
few additional triggers and thus the amount of secretion is lim-
ited. Once the meal is swallowed, on the other hand, meal con-
stituents trigger substantial release of gastrin and the physical

presence of the meal also distends the stomach and activates

stretch receptors, which provoke a “vago-vagal” as well as local

reflexes that further amplify secretion. The presence of the meal

also buffers gastric acidity that would otherwise serve as a feed-

back inhibitory signal to shut off secretion secondary to the

release of somatostatin, which inhibits both G and ECL cells as

well as secretion by parietal cells themselves (Figure 26–7). This

probably represents a key mechanism whereby gastric secretion

CLINICAL BOX 26–1

Peptic Ulcer Disease

Gastric and duodenal ulceration in humans is related primar-

ily to a breakdown of the barrier that normally prevents irrita-

tion and autodigestion of the mucosa by the gastric secre-

tions. Infection with the bacterium

Helicobacter pylori

disrupts this barrier, as do aspirin and other nonsteroidal

anti-inflammatory drugs (NSAIDs), which inhibit the produc-

tion of prostaglandins and consequently decrease mucus

and HCO

3

• secretion. The NSAIDs are widely used to combat
  pain and treat arthritis. An additional cause of ulceration is
  prolonged excess secretion of acid. An example of this is the
  ulcers that occur in the
  Zollinger–Ellison syndrome.
  This
  syndrome is seen in patients with gastrinomas. These tumors
  can occur in the stomach and duodenum, but most of them
  are found in the pancreas. The gastrin causes prolonged hy-
  persecretion of acid, and severe ulcers are produced. Gastric
  and duodenal ulcers can be given a chance to heal by inhibi-
  tion of acid secretion with drugs such as cimetidine that
  block the H
  2
  histamine receptors on parietal cells or omepra-
  zole and related drugs that inhibit H

• –K


• 
  

  ATPase.
  H. pylori
  can be eradicated with antibiotics, and NSAID-induced ulcers
  can be treated by stopping the NSAID or, when this is not ad-
  visable, by treatment with the prostaglandin agonist miso-
  prostol. Gastrinomas can sometimes be removed surgically.

  
  

FIGURE 26–4
Anatomy of the stomach.
The principal secre-
tions of the body and antrum are listed in parentheses.
(Reproduced
with permission from Widmaier EP, Raff H, Strang KT:
Vander’s Human Physiology: The
Mechanisms of Body Function
, 11th ed. McGraw-Hill, 2008.)

Esophagus

Body (secretes

mucus, pepsinogen,

and HCI)

Duodenum

Pyloric

sphincter

Antrum

(secretes

mucus,

pepsinogen,

and gastrin)

Fundus

Lower esophageal

sphincter

FIGURE 26–5

Structure of a gastric gland from the fundus

and body of the stomach.

These acid- and pepsinogen-producing

glands are referred to as “oxyntic” glands in some sources.

(Adapted

from Barrett KE:

Gastrointestinal Physiology

. McGraw-Hill, 2006.)

TABLE 26–1

Contents of normal gastric juice

(fasting state).

Cations: Na

+

, K

+

, Mg

2+

, H

+

(pH approximately 1.0)

Anions: Cl

• , HPO
  4
  2–
  , SO
  4
  2–

Pepsins

Lipase

Mucus

Intrinsic factor

Cell migration

Acid, intrinsic factor, pepsinogen

Mucus layer

Surface mucous cells

(mucus, trefoil peptide,

bicarbonate secretion)

Mucous neck cells

(stem cell compartment)

Parietal cells

(acid, intrinsic factor

secretion)

ECL cell

(histamine secretion)

Chief cells

(pepsinogen secretion)