TY - JOUR
T1 - Exogenous L-arginine does not affect angiotensin II-induced renal vasoconstriction in man
AU - Wolzt, Michael
AU - Ugurluoglu, Ara
AU - Schmetterer, Leopold
AU - Dorner, Guido
AU - Zanaschka, Gabriele
AU - Mensik, Christa
AU - Eichler, Hans Georg
PY - 1998
Y1 - 1998
N2 - Aims: It has been suggested that provision of the substrate of nitric oxide (NO) synthesis, L-arginine, might influence the effects of renal vasoconstrictors. We have therefore studied the effects of pretreatment or concomitant administration of L-arginine on angiotensin II (ANG II)-increased renovascular resistance. Methods: The study was conducted in a double-blind, randomized, cross-over design. Eight healthy subjects were assigned to placebo or a continuous intravenous coinfusion of ANG II (5.0 ng kg-1 min- 1, infusion period 75 min) with L-arginine (17 mg kg-1 min-1 infusion period 30 min). Nine further subjects received a continuous infusion of ANG II with or without pretreatment of L-arginine. Changes in renal plasma flow (RPF) were estimated by the steady state clearance of PAH. Results: L- arginine alone increased RPF to 110±10% over baseline (P<0.003). The ANG II- induced decrease in RPF was not affected by pretreatment or coinfusion of L- arginine. Conclusions: Our results demonstrate that a counterregulatory response of the renal vasculature to high levels of ANG II does not depend on exogenous L-arginine. In healthy subjects, this lack of functional antagonism at the renal vasculature is therefore not a result of NO substrate availability.
AB - Aims: It has been suggested that provision of the substrate of nitric oxide (NO) synthesis, L-arginine, might influence the effects of renal vasoconstrictors. We have therefore studied the effects of pretreatment or concomitant administration of L-arginine on angiotensin II (ANG II)-increased renovascular resistance. Methods: The study was conducted in a double-blind, randomized, cross-over design. Eight healthy subjects were assigned to placebo or a continuous intravenous coinfusion of ANG II (5.0 ng kg-1 min- 1, infusion period 75 min) with L-arginine (17 mg kg-1 min-1 infusion period 30 min). Nine further subjects received a continuous infusion of ANG II with or without pretreatment of L-arginine. Changes in renal plasma flow (RPF) were estimated by the steady state clearance of PAH. Results: L- arginine alone increased RPF to 110±10% over baseline (P<0.003). The ANG II- induced decrease in RPF was not affected by pretreatment or coinfusion of L- arginine. Conclusions: Our results demonstrate that a counterregulatory response of the renal vasculature to high levels of ANG II does not depend on exogenous L-arginine. In healthy subjects, this lack of functional antagonism at the renal vasculature is therefore not a result of NO substrate availability.
KW - Angiotensin II
KW - Nitric oxide physiology
KW - Reproducibility
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U2 - 10.1046/j.1365-2125.1998.00634.x
DO - 10.1046/j.1365-2125.1998.00634.x
M3 - Article
C2 - 9489597
AN - SCOPUS:0031929269
SN - 0306-5251
VL - 45
SP - 71
EP - 75
JO - British Journal of Clinical Pharmacology
JF - British Journal of Clinical Pharmacology
IS - 1
ER -