Disparate renal responses to arginine.HCl in patients with type-1 diabetes or essential hypertension: role of tubuloglomerular feedback

Abstract Ten control (C), 10 essential hypertensive (HT) and 9 type 1 diabetic (OM) subjects underwent renal hemodynamic studies of 3-hours infusion of 0.012 mmol.kg.min-1 L-arginine (ARG) buffered with equimolecular HCl. Mean Arterial Pressure, identical at baseline (8) in C and OM and -, 35% higher in HT (0.001), declined at the 3rd hour by 3.2% (0.001) in HT only. Glomerular Filtration Rate (GFR), identical at B in C and HT and 34% higher in DM (O.001), did not change in C and declined by 5.7 and 4.6% (0.001) in OM and HT. Renal blood flow, higher at B by 11% (0.02) in DM and lower by 9% (ns) in HT, rose by 23% in C (0.001) and to a significantly lesser extent (0.001 vs C) in both HT (+13%) and OM (+J 1%). Sodium excretion, identical in C, HT and OM at B, rose equally in C and HT (+95% and +103%, respectively) and much more in OM (+213%, 0.'001 vs both C and HT). Absolute Proximal Reabsorption (APR, GFR-clearance of exogenous lithium). slightly elevated at B in HT (13%, 0.05 vs C) and: much higher in DM (44%, 0.001), fell equally in C and HT (-15 and -19%, respectively) and much more in DM (-25%, '0.001 vs both C and HT). Renal hemodynamic response to. ARG.HCl is blunled similarly in HT and DM, with less vasodilation and decreased GFR, but tubular response is similar to C in HT and much more pronounced in DM. During ARG.HCI renal hemodynamic changes have been shown to be largely, modulated by an activation of tubuloglomerular feedbac (TGF) depending, on the natriuretic _ properties of buffering anion HCI (Biggi A et at, J Hypertens, 2007). Thus, the blunted vasodilatation in HT indicates an altered renal hemo-dynamic response to a normally activated TGF, while in DM, who show high GFR and APR with a deactivated TGF at S, an increased inhibition in tubular reabsorption during ARG.HCI. leading to both an exaggerated distal solute delivery and an abnormally activated TGF, seems to be responsible of the blunted renal vasodilation.