[Sites of action of CCK of the guinea pig gallbladder].
Cholecystokinin-octapeptide (CCK-OP) evoked contraction and 3H-acetylcholine (3H-ACh) release of the muscle strip of the guinea pig gallbladder were studied. Although hexamethonium (10(-5) M) or tetrodotoxin (10(-6) M) had no effect on CCK-OP (10(-8) M) evoked contraction and 3H-ACh release, Ca-free medium almost completely abolished CCK-OP (10(-8) M) evoked 3H-ACh release. In Ca-free medium contraction evoked by CCK-OP (10(-8) M) was reduced to about 84%, which fitted well with the calculated reduction observed in the presence of atropine (10(-6) M). Dibutyryl cyclic GMP (10(-3) M), which significantly reduced CCK-OP (10(-8) M) evoked contraction to about 40%, had no effect on CCK-OP (10(-8) M) evoked 3H-ACh release. CCK-OP receptors on the intramural cholinergic neurons might be suggested to be different from those on the muscle cells of the guinea pig gallbladder.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D003995:Dibutyryl Cyclic GMP / Q000494:pharmacology; D005260:Female; D005704:Gallbladder / Q000187:drug effects*; D006168:Guinea Pigs; D018738:Hexamethonium; D006584:Hexamethonium Compounds / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D012844:Sincalide / Q000494:pharmacology*; D013779:Tetrodotoxin / Q000494:pharmacology
D006584:Hexamethonium Compounds; D003995:Dibutyryl Cyclic GMP; D018738:Hexamethonium; D013779:Tetrodotoxin; D012844:Sincalide; D000109:Acetylcholine