The Effect of Corticotrophin-releasing Hormone (CRH) on Esophageal Motility in Healthy Volunteers
Status:
Completed
Trial end date:
2014-12-01
Target enrollment:
Participant gender:
Summary
Stress is well known to affect visceral sensitivity and gastrointestinal function in general.
A majority of patients with gastroesophageal reflux disease (GERD) report stress as an
important factor triggering symptom exacerbation. A real-life stressor could exacerbate
heartburn symptoms in GERD patients by enhancing perceptual response to esophageal acid
exposure. In Irritable Bowel Syndrome (IBS) patients, visceral hypersensitivity is a major
pathophysiological mechanism and stress is shown to trigger or exacerbate symptoms.
A possible mechanism of stress-induced visceral sensitivity could be the barrier dysfunction.
Indeed, in a study performed by our group, in human, an acute psychological stressor induces
hyperpermeability in a mast cell dependent fashion and exogenous peripheral
corticotrophin-releasing hormone (CRH) recapitulated its effects on barrier function. This
increase in intestinal permeability is a phenomenon which appears as a prerequisite for
visceral hypersensitivity. Furthermore, few studies indicate that human intestinal motility
is probably modulated by CRH. It has been shown that the brain-gut axis in IBS patients has
an exaggerated response to CRH.To our knowledge, the acute effect of exogenous CRH on
esophageal motility has not been studied before.