Search
Close
Search
Advanced Search
Search Menu
AI Discovery Assistant

Abstract

In order to investigate whether buffering anion plays a role in the renal effects of L-arginine (ARG)infusion in C and HTN humans, two 3-hours' infusion studies of .012 mmol.Kg.min-1 ARG- the first with 1.5 M HCl, the second with 1.5 M citric acid (CITR) as the buffer anion for ARG- were performed in 10 C and 10 untreated HTN on a 240 mM Na diet. Mean arterial pressure (MAP), GFR and RBF (inulin and PAH), fractional excretion of Na (FENa), Cl (FECl) and exogenous lithium (FELi) were measured for one hour at baseline and at each hour of infusion. Changes in cation excretion in C were opposite between HCl and CITR, with marked increase in FELi (+40%), FECl (+51%) and FENa (+95%) (.001 for all) under HCl and with decrease in FECl and FENa (-11% and-33%, .001 for both) and no change in FELi under CITR. Such changes were the same in HTN (p=ns). MAP decreased in C by 3% with CITR (.001) and did not change with HCl, while in HTN it fell with both HCl and CITR (-3% and -7%, .001 for both). GFR increased with CITR in C and HTN (+9.7 and +5.4%, .001 for both), while with HCl it did not change in C and declined in HTN (-4.6%, .05). RBF increased equally with CITR in C and HTN (+34, +33%, .001 for both) with no difference between the response curves (p=ns). With HCl, RBF also increased in C and HTN (+22 and +13%, respectively, .001 for both), although at a lesser extent than with CITR (.001 for both C and HTN). RBF response to HCl was significantly smaller in HTN than in C (by 41%, .001) and the difference in RBF response curve between CITR and HCl was greater in C than in HTN (.05). The present data show that the degree of renal hemodynamic response to ARG is different according to the accompanying anion, with much greater vasodilation with CITR than with HCl. Because ARG.HCl and not ARG.CITR inhibits tubular reabsorption, with consequent marked increase in NaCl distal delivery, these findings suggest that activation of TGF mediates the blunted hemodynamic response to ARG.HCl in comparison with ARG.CITR. Renal vasodilation is not impaired in HTN during ARG.CITR but it is with ARG.HCl which presumably activates TGF. This is consistent with the hypothesis that impaired nitric oxide- dependent, ARG-induced renal vasodilation observed by us and Others in HTN undergoing ARG.HCl infusion is explained by an abnormality in TGF-mediated glomerular hemodynamic regulation in HTN kidney.

L-Arginine, Kidney, Hypertension
This content is only available as a PDF.
© American Journal of Hypertension, Ltd. 2001
Topic:
Issue Section:
Abstracts
You do not currently have access to this article.
Download all slides