Do studies with ACE N- and C-domain-selective inhibitors provide evidence for a non-ACE, non-chymase angiotensin II-forming pathway?
Husain
Ahsan
A
Li
Ming
M
Graham
Robert M
RM
D000803:Angiotensin I / Q000378:metabolism; D000804:Angiotensin II / Q000096:biosynthesis*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001665:Binding Sites / Q000187:drug effects / Q000502:physiology; D001920:Bradykinin / Q000037:antagonists & inhibitors / Q000378:metabolism; D053818:Chymases; D006801:Humans; D018716:Molecular Mimicry; D009842:Oligopeptides / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000737:chemistry / Q000187:drug effects* / Q000502:physiology*; D017434:Protein Structure, Tertiary / Q000187:drug effects / Q000502:physiology; D012697:Serine Endopeptidases / Q000378:metabolism*; D013379:Substrate Specificity
D000806:Angiotensin-Converting Enzyme Inhibitors; D009842:Oligopeptides; D000804:Angiotensin II; D000803:Angiotensin I; D007703:Peptidyl-Dipeptidase A; D012697:Serine Endopeptidases; D053818:Chymases; C058504:goralatide; D001920:Bradykinin