5-Carboxamidotryptamine: a potent agonist mediating relaxation and elevation of cyclic AMP in the isolated neonatal porcine vena cava.

5-Carboxamidotryptamine (5-CT) caused concentration dependent relaxation of isolated rings from the porcine vena cava contracted with either prostaglandin F2 alpha, histamine or alpha-methyl 5-hydroxytryptamine. Relaxation was not inhibited by propranolol (l microM), atropine (1 microM), indomethacin (3 microM), mepyramine (1 microM), cimetidine (1 microM), or cocaine (10 microM). Methysergide, but not cyproheptadine, was a competitive antagonist of the relaxant effect of 5-CT with a pA2 value of 7.88. 5-Carboxamidotryptamine also increased the intracellular levels of cyclic AMP, an effect which was antagonised by methysergide (apparent pA2: 7.95) but not cyproheptadine. The alpha-methyl analogue of 5-hydroxytryptamine did not cause relaxation or elevate cyclic AMP. These results suggest that 5-CT causes relaxation and elevation of cyclic AMP by interaction with a specific 5-hydroxytryptamine receptor which is '5-HT1-like'.