Abstract
Mucosal cells were prepared by enzymatic digestion of porcine gastric mucosa with pronase and collagenase. The resulting cell suspension contained 10-15% parietal cells, which responded to histamine stimulation by an up to 20-fold increase in [14C]aminopyrine accumulation over control levels. Cholecystokinin-8 (CCK-8) evoked a more moderate stimulation of [14C]aminopyrine accumulation, whereas somatostatin inhibited histamine-stimulated accumulation. Parietal cells were enriched by elutriation and isopycnic centrifugation on density gradients of Percoll. A fraction with 60% parietal cells bound approximately three times more iodinated CCK-8 than a fraction containing 70% non-parietal cells. Binding of [125I]BH-CCK-8 to preparations containing 30-60% parietal cells was specifically inhibited to about 50% by 10(-9) M unlabelled CCK-8 but not by bombesin. Cell fractions containing about 30% parietal cells also bound [125I]somatostatin. Unlabelled somatostatin at 10(-9) M inhibited tracer binding by about 50%, while CCK-8 did not affect somatostatin binding to such a preparation. The results suggest the existence of specific receptors for CCK and somatostatin on porcine parietal cells exerting a regulatory influence on acid secretion.
Published Version
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