The involvement of bradykinin in virus-induced airway hyperresponsiveness (
AHR) in guinea pig airways in vivo was determined with the B-2-receptor ant
agonist Hoe 140. The efficacy of Hoe 140 treatment was assessed through its
effect on the bradykinin-induced (up to 2.5 mu g/100 g B.W. administered i
ntravenously) decrease in blood pressure (BP). Hoe 140 (0.1 mu mol/kg), adm
inistered subcutaneously twice a day for 5 d almost completely blocked brad
ykinin-induced changes in BP. Four days after parainfluenza-3 (PI-3) virus
infection, guinea pigs showed AHR; excessive airway contraction was found w
ith histamine-receptor stimulation. This hyperresponsiveness was completely
inhibited by pretreatment with Hoe 140 (0.1 mu mol/kg) administered subcut
aneously twice a day for five consecutive days, starting 1 d before virus i
noculation. Interestingly, nebulized delivery of bradykinin itself to capto
pril-treated animals induced an AHR comparable to that observed in virus-tr
eated guinea pigs. Viral infection also caused influx of bronchoalveolar ce
lls into the lungs. Both histologic: examinations and lung lavage experimen
ts showed that this cell influx could not be inhibited by pretreatment with
Hoe 140. In summary, the results of the study show that bradykinin is invo
lved in a cascade of events leading to AHR after a viral infection in guine
a pigs, without affecting bronchoalveolar cell influx.