title: [Are the radical scavenging properties of ACE inhibitors with sulfhydryl groups in therapeutically effective concentrations of quantitative significance?].
abstract: The chemiluminescence reaction elicited from luminol in the presence of hydroxyl radicals was concentration-dependently suppressed by captopril, indicating efficacious radical scavenging. As to be expected, ACE inhibitors lacking free sulfhydryl groups (ramipril, enalapril) were inactive. However, the endogenous scavenger and anti-oxidant uric acid proved to be far superior to captopril, when concentrations of both were compared that are realized in vivo. A substantial augmentation of endogenous scavenging ability during therapy with captopril thus seems unlikely. In a model of standardized myocardial hypoxia (isolated working heart of the guinea pig with 30 min low flow perfusion) captopril, ramiprilat and uric acid equally improved post-hypoxic heart function. There was no cardioprotective action of captopril in excess of that accountable for by inhibition of ACE. It seems possible that ACE (kininase II) inhibitors exert cardioprotection via elevated tissue levels of kinins: bradykinin also improved heart performance after low flow perfusion and bradykinin-induced coronary dilatation was markedly enhanced in the presence of ramiprilate, reflecting attenuated degradation by endothelial kininase II.
authors.affiliation: Physiologisches Institut Universität München.
authors.forename: B F
authors.initials: BF
authors.lastname: Becker
authors.forename: N
authors.initials: N
authors.lastname: Reinholz
authors.forename: B
authors.initials: B
authors.lastname: Leipert
authors.forename: P
authors.initials: P
authors.lastname: Raschke
authors.forename: E
authors.initials: E
authors.lastname: Gerlach
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D001643:Bridged Bicyclo Compounds / Q000494:pharmacology; D002216:Captopril / Q000494:pharmacology; D003327:Coronary Disease / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D004656:Enalapril / Q000494:pharmacology; D006168:Guinea Pigs; D006439:Hemodynamics / Q000187:drug effects; D006878:Hydroxides / Q000378:metabolism*; D017665:Hydroxyl Radical; D008163:Luminescent Measurements; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D011758:Pyrroles / Q000494:pharmacology; D017257:Ramipril / Q000031:analogs & derivatives; D013439:Sulfhydryl Reagents / Q000494:pharmacology*; D014527:Uric Acid / Q000494:pharmacology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D001643:Bridged Bicyclo Compounds; D006878:Hydroxides; D011758:Pyrroles; D013439:Sulfhydryl Reagents; D014527:Uric Acid; D017665:Hydroxyl Radical; D004656:Enalapril; C052549:ramiprilat; D002216:Captopril; D017257:Ramipril; D001920:Bradykinin
vernacular_title: Sind Radikalfänger-Eigenschaften von ACE-Inhibitoren mit Sulfhydrylgruppen bei therapeutisch wirksamen Konzentrationen von quantitativer Bedeutung?