1. One of the most important issues in the field of hypertension research centres on the therapeutic use of inhibitors of the renin-angiotensin system (RAS). Inhibitors of the RAS have potent anti-hypertensive effects, even in experimental models of hypertension and in human essential hypertension, where the activity of the peripheral RAS is low or normal. 2. It is suggested here that determining the mechanisms by which activation of the peripheral RAS produces hypertension will help us determine the anti-hypertensive effects of these inhibitors in low/normal renin-angiotensin hypertension. 3. Three hypotheses describing the hypertensive effects of angiotensin are discussed. The first hypothesis involves the direct vasoconstrictor effects of angiotensin. The second hypothesis suggests that chronic angiotensin produces hypertension by increasing Na+ reabsorption leading to volume expansion and hypertension. The final hypothesis suggests that, in angiotensin-induced hypertension, the increased Na+ reabsorption is not associated with volume expansion but, rather, is associated with an increase in vascular tone resulting from an interaction between angiotensin and the nervous system. 4. It is also hypothesized that the interaction between angiotensin and the nervous system produces a differential activation of sympathetic outflow that spares the kidney.