The formation of the vasoactive peptide angiotensin Il (ATT) is depend
ent on the sequential action of two enzymes, renin and angiotensin con
verting enzyme (ACE), on the substrate angiotensinogen, Although the r
enin-producing cells of the kidney do not express angiotensinogen, the
y contain large amounts of AII in the same storage granules that conta
in renin, When renin expression is suppressed in these cells, AII also
disappears, In the current study, me have tested whether the renin-as
sociated disappearance of AII in renal juxtaglomerular (JG) cells is d
ue to a renin-dependent down-regulation of granule biosynthesis and wh
ether receptor-mediated internalization of A1I could account for its c
oncentration in these cells, Our results support a model whereby AII p
eptides are generated within JG cells, presumably by a mechanism which
involves the action of endogenous renin on internalized, exogenous an
giotensinogen. (C) 1998 Federation of European Biochemical Societies.