Anxiogenic activity of intraventricularly administered bradykinin in rats.

The anxiogenic action of bradykinin was investigated in rats and compared with that of yohimbine, a known anxiogenic agent. Bradykinin (0.5, 1 and 2 μg/rat) was administered intracerebroventricularly (i.c.v.), whereas yohimbine (2 mg/kg) was administered i.p. The experimental methods used were the open- field, elevated plus-maze, social interaction and novelty suppressed feeding latency tests, and estimation of brain tribulin activity in terms of endogenous monoamine oxidase (MAO) A and MAO B inhibition. The behavioural and biochemical effects induced by bradykinin were qualitatively similar to those of yohimbine. Thus, both the drugs reduced ambulation and rears, and increased immobility and defecation, in the open-field test. They decreased the number of entries and time spent on the open arms of the elevated plus-maze, reduced social interaction in paired rats and increased the feeding latency in an unfamiliar environment in 48 h food-deprived rats. These effects are known to be associated with anxiety in animals. Bradykinin and yohimbine increased rat brain tribulin activity, the effect on the MAO A inhibitor component being more marked than that on the MAO B inhibitor component. The MAO A inhibitor component has been postulated to be the major anxiogenic moiety of tribulin. Lorazepam, a well known benzodiazepine anxiolytic agent, attenuated the anxiogenic effects of bradykinin and yohimbine, which may not be a functional effect. The investigation indicates that, like cholecystokinin (CCK), bradykinin may function as an endogenous anxiogenic peptide.