Cholinergic mechanism of sodium nicotinate-induced contractions in rat and guinea-pig descending colon.

In segments of rat descending colon 34.5 microM Na-nicotinate-induced rhythmic contractions that were late in onset, long lasting and reversible. The Na-nicotinate contractile effect was unaffected by 100 microM hexamethonium, whereas it was rapidly blocked by 30 nM scopolamine and inhibited by treating the samples with 20 microM hemicholinium-3, or 40 microM tetrodotoxin or 60 microM procaine, by incubation at 20 degrees C for 60 min or by removing CaCl2 from the incubation medium. In segments of rat descending colon exogenous acetylcholine induced an initial peak in developed tension followed by long lasting rhythmic contractions. Low indomethacin concentrations (from 3 to 60 microM) suppressed both Na-nicotinate and acetylcholine-initiated rhythmic contractile activity while a higher indomethacin concentration (0.6 mM) was required to abolish the acetylcholine-evoked first major contraction. Also in segments of guinea-pig descending colon 34.5 microM Na-nicotinate induced a contractile effect that was abolished by 30 nM scopolamine and almost completely absent in tissue samples treated with 20 microM hemicholinium-3 or exposed to low temperature. The data presented indicate that in segments of rat descending colon Na-nicotinate contractile activity is triggered by acetylcholine release from postganglionic nerve endings and that this cholinergic, calcium-dependent action appears to be modulated by a contemporary release of prostaglandin-like material. In addition, indication is given that this indirect mechanism can be responsible of the Na-nicotinate contractile action at the intestinal level in different animal species.