Impaired renal haemodynamic response to amino acid infusion in essential hypertension during angiotensin converting enzyme inhibitor treatment.

Abstract

To determine whether hyperfiltration induced by amino acid infusion can be influenced by angiotensin converting enzyme (ACE) inhibition. We studied the acute effects of ramipril in 12 healthy control subjects and in 14 patients with essential hypertension. We studied also the effects of 2 months' treatment with ramipril inn 12 patients with essential hypertension and performed a time-control study without amino acids infusion with 12 control subjects. The glomerular filtration rate (GFR), renal plasma flow (RPF), fractional excretion of sodium (FENa) and fractional excretion of lithium (FELi) were determined during 6 clearance periods of 30 min each and amino acids infusion was administered during the last four periods. Plasma concentrations of angiotensin II, aldosterone, atrial natriuretic peptide (ANP), arginine vasopressin, insulin and glucagon were determined. Both the GFR and the RPF increased markedly in healthy subjects after amino acid infusion both with (GFR 7%, RPF 7%) and without ramipril (GFR 7%), RPF 8%), both P < 0.05. Ramipril administered acutely to essential hypertensives prevented the amino acid-induced increase in RPF [with ramipril 5% (NS), without ramipril 9% (P < 0.05)]. The GFR increased equally with (5%) and without (8%) ramipril (P < 0.20). ACE inhibition after 2 months' treatment of essential hypertension blunted the amino acid-induced increase both in GFR and in RPF [with ramipril GFR 5% and RPF 3% (NS), without ramipril GFR 12%, RPF 11% (P < 0.05)]. The FENa did not change in all four experiments. The FELi, insulin and glucagon increased to the same extent in the first three experiments. ANP increased (P < 0.05) in control subjects both with and without ramipril; angiotensin II and aldosterone decreased significantly in control subjects without ramipril. The renal haemodynamic response both after acute and after short-term ACE inhibition is attenuated in essential hypertension. Presumably, this treatment makes the arterioles at the glomeruli unresponsive to subsequent amino acid infusion. This inhibition of hyperfiltration might be an important mechanism for the renal protective effect of ACE inhibition in some renal diseases.