bemesetron and 4-chlorophenylalanine-methyl-ester

Possible involvement of 5-hydroxytryptamine (5-HT), 5-HT receptors and prostaglandins in the acceleration of gastrointestinal transit by momordin Ic was investigated in mice. Accelerative effect of momordin Ic (25 mg/kg, p.o.) on gastrointestinal transit was attenuated by pretreatment with a bolus of DL-p-chlorophenylalanine methyl ester (an inhibitor of 5-HT synthesizing enzyme), but not repeated pretreatment with DL-p-chlorophenylalanine methyl ester. Furthermore, cyproheptadine (a nonselective 5-HT(2) receptor antagonist), ritanserin (a 5-HT(2A/2B/2C) receptor antagonist) and clozapine (a 5-HT(2A/2C) receptor antagonist) also attenuated the effect of momordin Ic, but methiothepin (a 5-HT(1) receptor antagonist), MDL 72222 (3-tropanyl-3,5-dichlorobenzoate) and metoclopramide (5-HT(3) receptor antagonists), tropisetron (a 5-HT(3/4) receptor antagonist), ketanserin and haloperidol (5-HT(2A) receptor antagonists) did not. These results suggested a possible involvement of endogenous 5-HT and 5-HT(2B/2C) over 5-HT(2A) receptors. Attenuation by pretreatment with indomethacin (an inhibitor of prostaglandins synthesis) suggested involvement of prostaglandins. It is postulated that momordin Ic accelerates gastrointestinal transit partially by stimulating synthesis of 5-HT to act through 5-HT(2), possibly 5-HT(2C) and/or 5-HT(2B) receptors, which, in turn, increases synthesis of prostaglandins.

Topics: Animals; Fenclonine; Gastrointestinal Motility; Indomethacin; Ketanserin; Male; Mice; Oleanolic Acid; Prostaglandins; Receptors, Serotonin; Serotonin; Tropanes