OBJECTIVE AND DESIGN: The aim of the present study was to examine the contribution of the two kinin receptors B1 and B2 to the increased blood flow observed in response to bradykinin (BK) in a blister model under different injury conditions. MATERIAL: Young male Sprague-Dawley rats weighing 250-350 g were used. METHODS: A vacuum-induced blister was raised in the rat hind paw and blood flow measured in the superfused blister base under four different conditions including, early phase acute injury; late phase acute injury; recurrent injury and early phase acute injury in the setting of chronic nerve damage. BK (10 microM) was superfused alone, or in the presence of the B1 antagonist DesArg9Leu8BK (DALBK), (10 nM) and/or the B2 antagonist [D-Arg,Hyp3,Thi5 D-Tic7,Oic8] Bradykinin (HOE 140) (10 nM). RESULTS: HOE 140 significantly inhibited the BK response in all models. Significant inhibition of BK-induced vasodilatation by DALBK was only observed in the late phase acute and recurrent injury models. CONCLUSIONS: The results suggest that the involvement of the inducible B1 receptor in skin inflammation site is related to the site, duration and recurrence of the injury condition.
OBJECTIVE AND DESIGN: The aim of the present study was to examine the contribution of the two kinin receptors B1 and B2 to the increased blood flow observed in response to bradykinin (BK) in a blister model under different injury conditions. MATERIAL: Young male Sprague-Dawley rats weighing 250-350 g were used. METHODS: A vacuum-induced blister was raised in the rat hind paw and blood flow measured in the superfused blister base under four different conditions including, early phase acute injury; late phase acute injury; recurrent injury and early phase acute injury in the setting of chronic nerve damage. BK (10 microM) was superfused alone, or in the presence of the B1 antagonist DesArg9Leu8BK (DALBK), (10 nM) and/or the B2 antagonist [D-Arg,Hyp3,Thi5 D-Tic7,Oic8] Bradykinin (HOE 140) (10 nM). RESULTS: HOE 140 significantly inhibited the BK response in all models. Significant inhibition of BK-induced vasodilatation by DALBK was only observed in the late phase acute and recurrent injury models. CONCLUSIONS: The results suggest that the involvement of the inducible B1 receptor in skin inflammation site is related to the site, duration and recurrence of the injury condition.