Oxidative stress may explain how hypertension is maintained by normal levels of angiotensin II

It is well known that essential hypertension evolves in most patients with "near normal" levels of plasma renin activity. However, these oxide levels appear to be responsible for the high levels of arterial pressure because t hey are normalized by the administration of angiotensin II converting inhib itors or angiotensin receptor antagonist. In experimental animals, hyperten sion can be induced by the continuous intravenous infusion of small doses o f angiotensin II that are not sufficient to evoke an immediate presser resp onse. However, this condition resembles the characteristics of essential hy pertension because the high levels of blood pressure exist with normal plas ma levels of angiotensin II. It is suggested that small amounts of angioten sin whose plasma levels are inappropriate for the existing size of extracel lular volume stimulate oxidative stress which binds nitric oxide forming pe roxynitrite, The latter compound oxidizes arachidonic acid producing isopro staglandin F2 alpha (an isoprostane) which is characterized by a strong ant inatriuretic vasoconstrictor renal effect. In this chain of reactions the v asoconstrictor effects derived from oxygen quenching of nitric oxide and in creased isoprostane synthesis could explain how hypertension is maintained with normal plasma levels of renin.