论文部分内容阅读
The present study examined whether or not the resistance to degradation of bradykinin analogs affects the kinin-potentiating action of the inhibitor of converting enzyme, perindoprilat. METHODS: Hydrolysis of [Hyp3,Tyr(Me)8]-bradykinin by ACE present in isolated canine coronary arteries was assessed by determination of peptide metabolites using electrospray mass spectrometry, and compared to that of bradykinin. Contractions and relaxations of isolated rings of coronary arteries, with and without endothelium, were recorded as changes in isometric force. RESULTS: After a 30 min incubation, most of the bradykinin was degraded by the arteries, while less than 10 % of [Hyp3 Tyr(Me)8]-bradykinin was hydrolysed. In organ chambers, [Hyp3, Tyr(Me)8]-bradykinin like bradykinin caused relaxations of isolated canine coronary arteries with endothelium that could be attributed to both NO and endothelium-derived hyperpolarizing factor (EDHF). Perindoprilat caused a comparable leftward shift in the concentration-relaxa
METHODS: Hydrolysis of [Hyp3, Tyr (Me) 8] -bradykinin by ACE present in isolated canine coronary arteries was assessed by determination of peptide metabolites using electrospray mass spectrometry, and compared to that of bradykinin. Contractions and relaxations of isolated rings of coronary arteries, with and without endothelium, were recorded as changes in isometric force. RESULTS: After a 30 min incubation of most of the bradykinin was degraded by the arteries, while less than 10% of [Hyp3 Tyr (Me) 8] -bradykinin was hydrolysed. In organ chambers, [Hyp3, Tyr (Me) 8] -bradykinin like bradykinin caused relaxations of isolated canine coronary arteries with endothelium that could be attributed to both NO and endothelium-derived hyperpolarizing factor (EDHF). Perindoprilat caused a comparable leftward shift in the co ncentration-relaxa