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ExtractAn investigation of the bradykinin system in cystic fibrosis of the pancreas was undertaken because of the potential role of bradykinin in the function of glandular tissues and in the mediation of electrolyte transport. Patients with cystic fibrosis of the pancreas (CFP) and control subjects (CS) were studied for evidence of excessive formation or impaired inactivation of bradykinin in plasma, saliva and urine. Bradykinin, kininase and kallikrein activities were assayed by means of a modified SchultzDale apparatus utilizing the uterus of rats in estrus.The bradykinin assay detected as little as 0.01 ,ug bradykinin (4 x ,ug/ml bath solution). The height of uterine contraction was proportional to the logarithmic concentration of bradykinin with maximum contraction occurring with 1-10 ,ug bradykinin.Free bradykininlike activity in urine, saliva or plasma specimens from 11 patients was the same as that from 21 normal controls. In saliva specimens from CFP or CS no bradykininlike activity was detected, whereas in urine there was slight activity in approximately 60% of the samples. Fresh heparinized plasma of both patients and controI subjects developed spontaneous bradykinin activity when added to the muscle bath; this type of activity could be prevented by shaking the plasma with glass beads and incubating at 37' for 30 min. All of the 'glass-shaken' plasma specimens developed normal-appearing bradykinin activity when activated by salivary kallikrein. The presence of bradykininlike activity in urine was unrelated to proteinuria since none of the patients with activity in their urine had detectable proteinuria. Five other patients with the nephrotic syndrome and heavy proteinuria had no bradykininlike activity in their urine.Plasma samples from 11 patients and 13 control subjects contained kininase that deactivated 10 pg synthetic bradykinin within 10 min. In each sample, salivary-induced bradykinin was similarly deactivated by the plasma kininase within 12 min. Urinary-induced bradykinin, however, was still present in many of the urine-plasma mixtures after 12 min, but in only two (one CFP and one CS) was there residual bradykinin activity after 22 min. Salivary kininase activity was detected in both patients and control subjects. Inactivation of 10 ,ug of synthetic bradykinin by 0.5 ml of saliva was much slower than that by plasma kininase and usually required up to 90 min. No kininase activity was detected in urine of patients or control subjects.Slight kallikrein activity was detected in urine of both groups. Kallikrein measured 1.95 f 1.7 units in 11 control subjects compared with 1.59 & 0.42 units in 8 patients. This difference was not significant. LIEBERMAN and LITTENBERGThe saliva from 11 patients showed a significantly greater kallikrein content (19.3 f 13 units) than that from 18 control subjects (7.2 f 8 units). I n patients, however, protein content was greater than in control subjects, and kallikrein activity correlated directly with the total protein content of the saliva ( r = 0.671 ; p .c 0.005...