Submitted on November 13, 2008
Revised on January 27, 2009
Accepted on March 2, 2009
Effects of repeated restraint stress on gastric motility in rats
Jun Zheng, Anthony Dobner, Reji Babygirija, Kirk Ludwig, and Toku Takahashi1*
1 Medical College of Wisconsin
* To whom correspondence should be addressed. E-mail: ttakahashi{at}mcw.edu.
In our daily life, individuals encounter with various types of stress. Accumulation of daily life stress (chronic stress) often causes GI symptoms and functional GI diseases. Although some can adapt toward chronic stress, the adaptation mechanism against chronic stress remains unknown. Although acute stress delays gastric emptying and alters upper GI motility, effects of chronic stress on gastric motility still remains unclear. We investigated the effects of acute (single stress) and chronic stress (repeated stress for 5 consecutive days) on solid gastric emptying and interdigestive gastroduodenal contractions in rats. It is well established that acute restraint stress inhibits solid gastric emptying via central corticotropin-releasing factor (CRF). To investigate whether the sensitivity to CRF is altered following chronic stress, CRF was administered intracisternally (ic). Ghrelin is involved to regulate gastric emptying and upper GI motility in rodents. The changes in plasma active ghrelin levels and mRNA expression in the stomach were studied following chronic stress. To evaluate the effects of chronic stress on hypothalamus-pituitary-adrenal (HPA) axis, plasma corticosterone levels were also measured. Delayed gastric emptying observed in acute stress was completely restored following chronic stress. Acute stress abolished gastric phase III-like contractions, without affecting duodenal phase III-like contractions in the interdigestive state. Impaired gastric phase III-like contractions were also restored following chronic stress. Plasma ghrelin levels and ghrelin mRNA expression were significantly increased after chronic stress. Ic-injection of CRF delayed gastric emptying and impaired gastric motility in rats who received chronic stress. Plasma corticosterone concentrations were no more elevated following chronic stress. The restored gastric emptying following chronic stress was antagonized by the administration of ghrelin receptor antagonists. The adaptation mechanism may involve upregulation of ghrelin expression and attenuation of HPA axis. In contrast, the sensitivity to central CRF remained unaltered following chronic stress in rats.
