Angiotensin I-converting enzyme kininase II; ACE inhibitors, antibodies to
ACE and slowly cleaved substrates of ACE potentiate the effect of bradykini
n and its analogs on their B-2, receptors independently of blocking peptide
metabolism. ACE inhibitors also resensitized the receptors desensitized by
the ligand (tachyphylaxis). The studies were performed on isolated organs
and cells co-transfected with the receptor and the enzyme or constitutively
expressing them. This enhancement of the effect of B-2, ligands is attribu
ted to a crosstalk between the enzyme and the receptor and not to a direct
action on the receptors. It might reflect some of the local activities of A
CE inhibitors.