Th ere is increasing evidence for the interplay of the renin-angiotensin system and infl ammatory events [5] . Pre-eclampsia is associated with circulating autoantibodies against the AT 1 protein that act as functional receptor agonists to promote vasoconstriction and infl ammation [5] . Studies by Harrison and colleagues suggest that T-cell expression of the AT 1 receptor contributes to infl ammatory events and the development of hypertension. Moreover, activated T cells may themselves generate Ang II locally to infl uence cell function in an autocrine manner [6] . In experimental encephalo myelitis, AT 1 expression was increased and subsequent AT 1 receptor blockade or ACE inhibition ameliorated the autoimmune infl ammation [7] .