No abstract

Membrane fragments of isolated cells from guinea pig gastric mucosa, enriched to 65% parietal cells, bind with high affinity the opioid peptide ³H-D-Ala²-D-Leu⁵-enkephalin (³H-DADLE). Binding was saturable and reversible. Scatchard analysis revealed a second binding site with low affinity but high capacity. Acid secretion by isolated, enriched parietal cells was determined by means of ¹⁴C-aminopyrine uptake. Basal acid secretion was not influenced by DADLE but that stimulated by histamine was further augmented by the enkephalin analog. This potentiating effect was prevented by the opioid antagonist naloxone. The present data provide for the first time evidence that gastric acid secretion is modulated by an opioid mechanism probably located on the parietal cell.

Acid secretion from isolated and enriched guinea-pig parietal cells stimulated by histamine and measured by the ¹⁴C-aminopyrine accumulation technique was enhanced by nanomolar concentrations of D-ala²-D-leu⁵-enkephalin (DADLE). This effect was blocked by naloxone. Naloxone inhibited histamine-stimulated acid secretion even in the absence of exogenous opioids. The effect of naloxone was stereospecific, i.e. (+)-naloxone was ineffective. The DADLE effect varied between different cell preparations and changed from stimulation to inhibition as the inhibitory effect of naloxone alone increased. Thus, an inverse relationship between the magnitude of inhibition by naloxone and enhancement by DADLE was observed. The data suggest that endogenous opioids modulate acid secretion in gastric muco-sal cells.

No abstract