Cholecystokinin-induced contraction of dispersed smooth muscle cells.
Isolated smooth muscle cells were prepared from the fundus of guinea pig stomach by incubation with collagenase. Incubating the cells with the C-terminal octapeptide of cholecystokinin induced contraction, which was measured by micrometry and expressed as percent decrease in mean cell length. Cholecystokinin-induced contraction was maximal within 30 s and reduced cell length by approximately 37%. The threshold concentration of cholecystokinin was 0.1 pM, and the maximally effective concentration was 0.3 nM. Contraction caused by cholecystokinin could be inhibited by proglumide and by glucagon. Inhibition by proglumide was competitive and resulted in a parallel rightward shift of the cholecystokinin dose-response curve. In contrast, inhibition by glucagon was noncompetitive and resulted in a reduction in the efficacy of cholecystokinin without a change in its potency. Furthermore, proglumide-induced inhibition was specific for cholecystokinin, whereas glucagon-induced inhibition of contraction was nonspecific and reduced the contraction caused by carbamylcholine and the calcium ionophore A23187.
D000818:Animals; D001067:Appetite Depressants / Q000494:pharmacology; D001693:Biological Transport, Active; D000001:Calcimycin / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D002766:Cholecystokinin / Q000494:pharmacology*; D005934:Glucagon / Q000494:pharmacology; D006168:Guinea Pigs; D007700:Kinetics; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects / Q000502:physiology*; D010446:Peptide Fragments / Q000494:pharmacology; D011377:Proglumide / Q000494:pharmacology; D012413:Rubidium / Q000378:metabolism; D012844:Sincalide; D013270:Stomach / Q000502:physiology*
D001067:Appetite Depressants; D010446:Peptide Fragments; D000001:Calcimycin; D002217:Carbachol; D005934:Glucagon; D002766:Cholecystokinin; D011377:Proglumide; D012844:Sincalide; D012413:Rubidium