The nonapeptide bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) and the decapeptide kallidin (Lys-bradykinin) are released during tissue damage and cause vasodilation, increased vascular permeability, altered gut motility and pain1-4. Accordingly, they have been implicated in several pathological processes, including carcinoid tumours and postgastrectomy dumping syndrome. Symptoms of these two syndromes include flushing, light-headedness, headaches and diarrhoea5-9. Increased blood levels of bradykinin 5,7-9 and kallikrein9, the bradykinin-releasing enzyme, have been noted in such patients and may explain these symptoms. However, while kinin-forming and -destroying activity has been noted in the gut 10-14, bradykinin itself has not been directly demonstrated. Moreover, while bradykinin influences gut motility and electrical activity 15,25,26, most clinical diarrhoea is due to ion and fluid secretion into the gut lumen rather than altered motility16. We describe here specific bradykinin receptors in intestinal mucosa and muscle. We also report that bradykinin and several peptide analogues potently stimulate chloride secretion in the gut with a peptide specificity indicative of specific receptor interactions. These findings suggest a physiological and a pathological role for kinins in intestinal function. Throughout this report the term kinin will indicate both bradykinin and kallidin activities since in several cases the true active form is unknown.
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