Water-avoidance stress enhances gastric contractions in freely moving conscious rats: role of peripheral CRF receptors

Abstract

Stress alters gastrointestinal motility through central and peripheral corticotropin-releasing factor (CRF) pathways. Accumulating evidence has demonstrated that peripheral CRF is deeply involved in the regulation of gastric motility, and enhances gastric contractions through CRF receptor type 1 (CRF1) and delays gastric emptying (GE) through CRF receptor type 2 (CRF2). Since little is known whether water-avoidance stress (WAS) alters gastric motility, the present study tried to clarify this question and the involvement of peripheral CRF receptor subtypes in the mechanisms. We recorded intraluminal gastric pressure waves using a perfused manometric method. The rats were anesthetized and the manometric catheter was inserted into the stomach 4-6days before the experiments. We assessed the area under the manometric trace as the motor index (MI), and compared this result with those obtained 1h before and after initiation of WAS in nonfasted conscious rats. Solid GE for 1h was also measured. WAS significantly increased gastric contractions. Intraperitoneal (ip) administration of astressin (100μg/kg, 5min prior to stress), a nonselective CRF antagonist, blocked the response to WAS. On the other hand, pretreatment (5min prior to stress) with neither astressin2-B (200μg/kg, ip), a selective CRF2 antagonist, nor urocortin 2 (30μg/kg, ip), a selective CRF2 agonist, modified the response to WAS. These drugs did not alter the basal MI. WAS did not change GE. WAS may activate peripheral CRF1 but not CRF2 signaling and stimulates gastric contractions without altering GE.