During the past decade many investigators have used plasma renin activity (PRA) to subgroup or "classify" patients with essential hypertension. The yield in clinical terms has been disappointing. Plasma renin activity has failed to consistently reflect prognosis, to accurately predict response to therapy, or even to adequately screen for renovascular hypertension. Paradoxically, it has also become increasingly evident that the renin-angiotensin-aldosterone system is intimately involved in the pathophysiology of the hypertensive state. Results of recent studies that used specific angiotensin-II (AII) blockade demonstrate a probable role for AII in most patients with essential hypertension.1 The degree of AII dependence appears to be proportional to PRA. The implication is that patients with low and high PRA differ fundamentally in regard to the mechanism of their hypertension. Why, then, do they not differ clinically as well?
The simplest conclusion, ie, that the mechanism of hypertension is not an important determinant of