Lecture 29- Friday, March 19 , 2010h
1. Normal HCl output
Weak barrier (agents responsible: Aspirin and NSAIDs, Heliobacter pylori)
2. Normal Barrier
Excessive HCl output (eg: Gastrin producing factors)
Phases of Gastric Secretion:
Cephalic psychic, gustatory
Cephalic Phase (Vagally-mediated)
-All regulatory cells are secreting. Accompanied by vasodilation. Distension leads to short intramural reflexes. Also results in afferent fibres going up
and efferent fibres as well. Called vagal-vagal reflex.
GASTRIN is released in response to:
a) SECRETAGOGUES (products of protein digestion) (Antrum Lumen)
b) Local enteric reflexes
c) Vagally-mediated reflexes Physiological Role of Gastrin
a) HCl secretion
b) Trophic effect
Lots of Histamine in gastric mucosa.
Histamine administration elicits large volume of gastric juice with lots of HCl. PERMISSIVE HYPOTHESIS (Paracrine Fashion)–
Histamine is constantly released and presented to the Parietal Cells as a tonic
background, sensitizing them to other stimuli.
Blocking this tonic background by H2-antagonists, inhibits acid secretion in response
to ACh and Gastrin. (H+/K+ ATPase, eg: Nexium)
H2 blockers are widely used to decrease HCl secretion (eg: Pepsid).
Intestinal Phase Intestinal Phase – Inhibitory Optimal secretory activity is the result of an interplay between neural and
hormonal mechanisms. Gastri