Among the main bioactive peptides of the brain renin-angiotensin system, an
giotensin (Ang) II and AngIII exhibit the same affinity for type 1 and type
2 AngII receptors, Both peptides, injected intracerebroventricularly, caus
e similar increases in vasopressin release and blood pressure. Because AngI
I is converted in vivo to AngIII, the identity of the true effector is unkn
own. This review summarizes new insights into the predominant role of brain
AngIII in the control of vasopressin release and blood pressure and underl
ines the fact that brain aminopeptidase A, the enzyme forming central AngII
I, could constitute a putative central therapeutic target for the treatment
of hypertension.