Previous studies have demonstrated that β-endorphin and enkephalins are released into the systemic circulation by the pituitary and adrenal medulla, respectively. To determine whether the small intestine could be a target for circulating β-endorphin, segments of small intestine were removed from anesthetized dogs and perfused with Krebs-bicarbonate buffer containing β-endorphin (1 μg/ml), while motility was recorded and venous effluent collected in 1-min fractions (23 ml). β-Endorphin significantly (P < .002) increased motility of intestinal segments. High-performance liquid chromatographic analysis of the venous effluent identified, among others, several α- and γ-type endorphins. Several of the identified peptide fragments were then perfused through intestinal segments to determine their motility effects. α-Endorphin, γ-endorphin, des-tyrosine-α-endorphin and des-tyrosine-γ-endorphin, significantly increased motility at doses of 1 μg/ml. These responses were characterized by an increase in phasic contractions of constant amplitude and frequency. To determine regional specificity and site of β-endorphin metabolism during perfusion, the authors studied time course processing of β-endorphin in mucosal and muscularis homogenates in vitro. The mucosa was much more enzymatically active than the muscularis and produced 3-fold more γ-endorphin than α-endorphin, whereas the reverse was found in the muscularis. These studies demonstrate that the small intestine can metabolize β-endorphin into a number of active fragments which increase motility and suggest a regional specificity of enzymatic processing of β-endorphin in the dog intestine.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Pharmacology and Experimental Therapeutics|
|State||Published - Dec 1 1983|
ASJC Scopus subject areas
- Molecular Medicine