Regulation of duodenal bicarbonate secretion during stress by corticotropin-releasing factor and beta-endorphin.

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Abstract
Proximal duodenal muscosal bicarbonate secretion is an important factor in the pathogenesis of duodenal ulcer disease. To examine the central nervous system regulation of duodenal bicarbonate secretion, an animal model was developed that allowed cerebroventricular and intravenous injections as well as collection of duodenal perfusates in awake, freely moving rats. The hypothalamic peptide corticotropin-releasing factor (CRF) and stress (physical restraint) significantly stimulated duodenal bicarbonated secretion. These responses were abolished by pretreatment of the animals with the CRF receptor antagonist .alpha.-helical CRF-(9-41), hypophysectomy, and naxolone. In contrast, blockade of autonomic efferents by surgical and pharmacological means did not prevent the stimulatory effects of stress and CRF. Intravenous, but not cerebrovascular, administration of .beta.-endorphin that produced plasma concentrations of .beta.-endorphin that were similar to those produced by exogenous CRF and stress significantly stimulated duodenal bicarbonated secretion. These results indicated that endogenous CRF release during stress and exogenously administered CRF stimulated duodenal bicarbonate secretion by release of .beta.-endorphin from the pituitary, thus, demonstrating a functional hypothalamus-pituitary-gut axis.