It depends on what condition you're talking about. In primary HTN, renal perfusion pressure and thus GFR is increased due to the systemic HTN. Therefore, the GFR is less dependent on the effect of angiotensin II because you can imagine that the kidneys are "feeling" the systemic high blood pressure. However, in renovascular HTN, renal perfusion pressure is decreased due to a stenotic lesion. This decrease leads to upregulation of renin which then increases angiotensin II. This leads to constriction of the efferent arteriole to increase renal perfusion pressure and thus GFR thus compensating for the flow-limiting lesion in the renal artery.
So if you give someone with primary HTN an ACE inhibitor, you're not going to see much of a change in GFR because renin/angiotensin isn't upregulated to begin with and the kidneys can just compensate. But someone with renovascular HTN is dependent on angiotensin II to maintain their GFR. So if you give them an ACE inhibitor, you're going to reduce the renal perfusion pressure via the systemic BP lowering effect of ACEi's and because you're also blocking angiotensin II formation, they lose the only compensating mechanism they have. So now since they can't constrict the efferent arteriole to increase GFR, GFR decreases and you can precipitate AKI.
Look up the UptoDate article on "Renal effects of ACE inhibitors in hypertension."
