I'm sure it inhibits the emptying of the stomach. However many sources claim that it is done by contraction of the muscles, and others say that its due to relaxation via vagovagal reflex.
Well, I don't know about the stomach, but some studies on the gallbladder show that CCK dose-dependently increases the amplitude of EPSPs and evokes action potentials in gallbladder neurons. This effect is already measurable at 20 pM and blocked by a CCK1 (not CCK2) antagonist (Mawe 1991, J. Physiol. 439: 89).
Vagotomy of the gallbladder prevents the stimulatory effects of CCK on gallbladder contraction (Takahashi et al. 1991, Am. J. Physiol. 261: G565). In a review Mawe proposes that vagal preganglionic cholinergic neurons are a target for hormonal CCK (1998, News Physiol. Sci. 13: 84).
So, the vagal nerve as a target in the CCK-induced enterogastrone effects seems a plausible mechanism.
The most convincing mechanism I've found is CCK causing
1) relaxation of the muscles of the distal part of stomach BUT
2) contraction of the pyloric sphincter
Those two certainly contribute to the main action of CCK, which is inhibition of gastric emptying, and lack of which is observed using CCK1 antagonists like loxiglumide.
However, as I see, the physiological basis is still being described and waiting for full explanation
Contraction patterns of the smooth muscle layers of the stomach differ greatly from the oral (fundus) to the aboral (pylorus) parts, so it is not at all that contradictory to suppose different effects of CCK in the distal (antral) and pyloric regions of the stomach.
Effect of cholecystokinin on gastric motility in humans.
Beglinger C.
Ann N Y Acad Sci. 1994 Mar 23;713:219-25. Review.
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