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10.1111/1440-1681.12212

http://scihub22266oqcxt.onion/10.1111/1440-1681.12212
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C3973160!3973160 !24472006
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suck abstract from ncbi

pmid24472006
      Clin+Exp+Pharmacol+Physiol 2014 ; 41 (4 ): 270-8
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  • Exogenous L-arginine attenuates the effects of angiotensin II on renal hemodynamics and the pressure natriuresis-diuresis relationship #MMPMID24472006
  • Das S ; Mattson DL
  • Clin Exp Pharmacol Physiol 2014[Apr]; 41 (4 ): 270-8 PMID24472006 show ga
  • Administration of exogenous L-arginine (L-Arg) attenuates angiotensin-II (AngII)-mediated hypertension and kidney disease in rats. The present study assessed renal hemodynamics and pressure diuresis-natriuresis in anaesthetized rats infused with vehicle, AngII (20 ng/kg per min i.v.) or AngII + L-Arg (300 ?g/kg per min i.v.). Experiments in isolated aortic rings were carried out to assess L-Arg effects on the vasculature. Increasing renal perfusion pressure (RPP) from ~100 to 140 mmHg resulted in a nine- to tenfold increase in urine flow and sodium excretion rate in control animals. In comparison, AngII infusion significantly reduced renal blood flow (RBF) and glomerular filtration rate (GFR) by 40-42%, and blunted the pressure-dependent increase in urine flow and sodium excretion rate by 54-58% at elevated RPP. Supplementation of L-Arg reversed the vasoconstrictor effects of AngII and restored pressure-dependent diuresis to levels not significantly different from control rats. Dose-dependent contraction to AngII (10(-10) mol/L to 10(-7) mol/L) was observed with a maximal force equal to 27 ± 3% of the response to 10(-5) mol/L phenylephrine. Contraction to 10(-7) mol/L AngII was blunted by 75 ± 3% with 10(-4) mol/L L-Arg. The influence of L-Arg to blunt AngII-mediated contraction was eliminated by endothelial denudation or incubation with nitric oxide synthase inhibitors. Furthermore, the addition of 10(-3) mol/L cationic or neutral amino acids, which compete with L-Arg for cellular uptake, blocked the effect of L-Arg. Anionic amino acids did not influence the effects of L-Arg on AngII-mediated contraction. These studies show that L-Arg blunts AngII-mediated vascular contraction by an endothelial- and nitric oxide synthase-dependent mechanism involving cellular uptake of L-Arg.
  • |Angiotensin II/metabolism/*pharmacology [MESH]
  • |Animals [MESH]
  • |Arginine/*pharmacology [MESH]
  • |Diuresis/*drug effects/physiology [MESH]
  • |Glomerular Filtration Rate [MESH]
  • |Hemodynamics/*drug effects/physiology [MESH]
  • |Kidney/blood supply/*drug effects/physiology [MESH]
  • |Natriuresis/*drug effects/physiology [MESH]
  • |Rats [MESH]


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