The hemoregulatory peptide N-acetyl-ser-asp-lys-pro impairs angiotensin I-induced contractions in rat aorta

The hemoregulatory peptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is degraded by ACE. This study was designed to examine the effect of Ac-SDK P on the contractions to angiotensin I. Experiments were performed on rat a ortic rings with endothelium exposed to nitro-L-arginine. Ac-SDKP (10 and 1 00 mu M) significantly augmented angiotensin I ED20 (from 2.0 +/- 0.4 to 4. 2 +/- 1.0 and 5.0 +/- 0.9 nM) and ED50 (from 4.3 +/- 0.7 to 8.6 +/- 1.0 and 10.7 +/- 1.3 nM, respectively), but did not alter its maximal response. Th e contractions to angiotensin II were not affected by Ac-SDKP. No degradati on of exogenous Ac-SDKP nor detectable release of endogenous Ac-SDKP were o bserved in the incubation medium. These results suggest that Ac-SDKP impair s angiotensin I response by inhibiting ACE and subsequent angiotensin II fo rmation. (C) 1998 Elsevier Science B.V. All rights reserved.