Tissue renin: focus on vascular angiotensin formation.

Abstract

Local vascular formation of angiotensin (Ang) peptides was investigated in isolated, plasma-free perfused rat hindquarters. Analysis of perfusate by high performance liquid chromatography and radioimmunoassay demonstrated spontaneous releases of Ang I and II from hindlimb vasculature. Captopril suppressed Ang II and increased Ang I levels. Formation of Ang peptides was abolished by bilateral nephrectomy but unaltered by subtotal 5/6 nephrectomy. Infused renin was taken up by hindlimb vasculature and led to substantial increases of local Ang formation and perfusion pressure. Both effects were sensitive to captopril (CAS 62571-86-2) and to the renin inhibitor H-142 (H-Pro-His-Pro-Phe-His-Leu-Val-Ile-His-OH). Conversion of Ang I to Ang II in hindquarter vasculature was approximately 75% and completely suppressed by captopril. Evidence for and against local vascular synthesis of renin is briefly discussed. In conclusion, the data indicate substantial local vascular formation of Ang I and II which, however, appears to be mainly due to plasma-derived renin.

Cite this paper

@article{Hilgers1993TissueRF, title={Tissue renin: focus on vascular angiotensin formation.}, author={Karl Friedrich Hilgers and Jill F. Mann}, journal={Arzneimittel-Forschung}, year={1993}, volume={43 2A}, pages={198-201} }