Impaired Renal Hemodynamic Response to L- Arginine in Essential Hypertensive Humans : Role of buffering anion and tubuloglomerular feedback

Abstract Objective To investigate whether changes in tubuloglomerular feedback (TGF) dependent upon the tubular effects of buffering anions affect the renal haemodynamic response to L-arginine in healthy (control) individuals and patients with essential hypertension. Methods Mean arterial pressure (MAP), glomerular filtration rate (GFR), renal blood flow (RBF) and fractional excretion of sodium (FENa), chloride (FECl) and lithium (FELi) were measured in 10 control individuals and 10 hypertensive patients during two 3-h infusions of 0.012 mmol/kg per min L-arginine buffered with either HCl or citric acid. Results FELi, FECl and FENa increased (P<0.001) comparably in controls and hypertensive individuals with arginine–HCl and decreased with arginine–citrate (P<0.001). MAP was unchanged in controls with arginine– HCl and decreased by 3% with arginine–citrate (P<0.001), and decreased in hypertensive individuals with both arginine–HCl and arginine–citrate (by 3 and 7%, respectively; P<0.001). GFR increased with arginine– citrate in controls and hypertensive individuals (by 6.1 and 5.4%, respectively; P<0.001), but did not change with arginine–HCl in controls and declined by 4.6% in hypertensive individuals (P<0.05). RBF increased equally after arginine–citrate in controls and hypertensive individuals (by 34 and 33%, respectively; P<0.001); it also increased after arginine–HCl (22 and 13%, respectively; P<0.001), but less than after arginine–citrate (P<0.001),