作者: Monica C.Y. Chen , Deborah A. Amirian , Mary Toomey , Martin J. Sanders , Andrew H. Soll
DOI: 10.1016/0016-5085(88)90002-9
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摘要: Abstract We have investigated the mechanisms underlying prostaglandin inhibition of histamine-stimulated parietal cell function. Enzyme-dispersed canine cells were enriched by elutriation. The accumulation weak base [ 14 C]aminopyrine was used as an index function and cyclic adenosine monophosphate content measured radioimmunoassay. Step density gradients elutriator-enriched fractions indicated that accounted for histamine stimulation production E analogue Enprostil. Pertussis toxin diphosphate-ribosylates a subunit with molecular weight 41,000, thereby inactivating inhibitory guanine nucleotide-binding protein adenylate cyclase. treatment in over-night suspension culture to determine if guanosine triphosphate-binding mediated prostanoid inhibition. In control cultured cells, 2 Enprostil markedly inhibited forskolin- aminopyrine accumulation. treated pertussis (300 ng/ml) 18 h, histamine, isobutylmethyl-xanthine, forskolin unaltered compared whereas reduced. toxin-treated generation unaltered, membranes from control, but not toxin-treated, induced 32 P]adenosine diphosphate-ribosylation membrane presumably α-subunit protein. conclude prostanoids inhibit receptor-mediated interaction nucleotidebinding