BLOOD-PRESSURE REDUCTION INITIATES THE ANTIPROTEINURIC EFFECT OF ACE-INHIBITION

Several observations question the role of blood pressure and renal hem odynamic changes in the long-term antiproteinuric effect of ACE inhibi tion. To differentiate blood pressure and renal effects in the initial antiproteinuric response, the placebo-controlled acute effects of the ACE inhibitor enalaprilat (10 mg i.v.) on blood pressure, renal hemod ynamics, and proteinuria were compared with those of nitroprusside in nine patients with non-diabetic proteinuria. In addition, we studied w hether an exogenous angiotensin II infusion reverse the initial enalap rilat-induced antiproteinuric response. Enalaprilat and nitroprusside reduced MAP by -11.3 +/- 2.4% and -14.1 +/- 2.3%, respectively, wherea s only enalaprilat showed renal hemodynamic effects, reflected by an i ncrease in ERPF of 18.4 +/- 5.4% and a decrease in FF of -17.1 +/- 2.6 %. Despite the contrasting renal hemodynamic profiles, enalaprilat (-1 0.6 +/- 4.8%) and nitroprusside (-12.8 +/- 5.1%) equally decreased pro teinuria. Exogenous infusion of angiotensin II completely reversed the blood pressure reduction and renal efferent vasodilatation induced by enalaprilat. Proteinuria also increased by 13.1 +/- 7.8% to placebo l evel, albeit statistically non-significant. We conclude that the initi al antiproteinuric effect of ACE inhibition appears to be mediated by blood pressure reduction and does not require its specific renal hemod ynamic effect. Further studies should clarify whether the renal effere nt vasodilatation during ACE inhibition is required to gradually induc e renal structural changes that prevent the abundant passage of protei ns.