From the Guidelines
The answer is (c) epinephrine, as it inhibits intestinal motility by binding to alpha-2 and beta-2 adrenergic receptors in the gastrointestinal tract, causing relaxation of smooth muscle and decreased contractility 1. This inhibitory effect is part of the body's "fight or flight" response, where digestive functions are temporarily suppressed during stress or emergency situations to divert blood flow and energy to more critical systems like skeletal muscles and the heart.
Comparison with Other Options
In contrast, the other options actually stimulate intestinal motility:
- Gastrin promotes gastric motility
- Cholecystokinin stimulates pancreatic enzyme secretion and gallbladder contraction
- Motilin initiates the migrating motor complex between meals
- Serotonin generally enhances intestinal contractions through 5-HT receptors in the enteric nervous system, as seen with the use of 5HT 4 receptor agonists like prucalopride, which has prokinetic properties 1.
Clinical Implications
The management of intestinal motility disorders often involves the use of prokinetic agents, such as metoclopramide, domperidone, and erythromycin, which can help improve gastrointestinal motility and alleviate symptoms like vomiting and constipation 1. However, the use of these agents should be carefully considered, as they can have significant side effects and interactions. In the context of inhibiting intestinal motility, epinephrine is a key player, and its effects should be taken into account when managing patients with intestinal motility disorders.
From the Research
Inhibition of Intestinal Motility
The following substances have been found to inhibit intestinal motility:
- Epinephrine: A study published in 1976 found that adrenaline (epinephrine) inhibits intestinal motility by uncoupling the control activity to response activity through suppression of the prepotentials 2.
- Cholecystokinin (CCK): While CCK is known to stimulate intestinal motility, a study published in 2005 found that psychological stress down-regulates CCK expression in the small intestine, leading to inhibited small intestinal transit 3.
- Serotonin: Depending on the receptor subtype, serotonin can have either progastric or antigastric motility effects. However, serotonin receptor agonists have been used clinically to treat dyspepsia symptoms, suggesting that serotonin can inhibit gastric motility under certain conditions 4.
- Vasoactive intestinal polypeptide (VIP): A study published in 2005 found that psychological stress up-regulates VIP expression in the small intestine, leading to inhibited small intestinal transit 3.
- Noradrenaline: As the primary transmitter of sympathetic neurones that supply the intestine, noradrenaline can inhibit intestinal motility 5.
Substances with No Clear Inhibitory Effect
The following substances do not have a clear inhibitory effect on intestinal motility:
- Gastrin: There is no evidence to suggest that gastrin inhibits intestinal motility.
- Motilin: Motilin is known to promote gastric motility, particularly during fasting 4.
- Substance P: While substance P can stimulate and inhibit intestinal peristalsis via distinct receptors, its overall effect on intestinal motility is complex and dependent on the specific receptors involved 6.