Effects of amino acid infusion on renal hemodynamics role of endothelium-derived relaxing factor

Jonathan P. Tolins, Leopoldo Raij

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

Ingestion of protein or intravenous infusion of amino acids acutely elevates glomerular filtration rate (GFR) and renal plasma flow (RPF) by unknown mechanisms. Endothelium-derived relaxing factor (EDRF), now known to be nitric oxide derived from metabolism of L-arginine, participates in local regulation of vascular tone. To investigate the hypothesis that EDRF may participate in the renal vasodilatation and increased GFR after amino acid infusion, we characterized the effect of inhibition of EDRF synthesis with NG-monomethyl L-arginine (LNMMA) on basal renal hemodynamics and the response to infusion of a 10% mixed amino acid solution (1 ml/hr i.v.) in the rat. Renal arterial infusion of LNMMA (500 μg/kg/min) resulted in a significant increase in mean arterial pressure, decreases in GFR (20%) and RPF (44%), and a significant increase in filtration fraction. Pretreatment with the angiotensin II receptor antagonist Sar-Gly-angiotensin II did not prevent the increase in blood pressure but blunted the decreases in GFR (11%) and RPF (27%) after LNMMA infusion. Amino acid infusion in the untreated, fasted rat resulted in no change in blood pressure but significant increases in GFR and RPF; these effects were completely inhibited by intrarenal LNMMA but not an equihypertensive intravenous infusion of phenylephrine. In summary, EDRF participates in regulation of basal renal hemodynamics. Furthermore, amino acid-induced hyperfiltration and renal vasodilatation are completely prevented by inhibition of EDRF synthesis. We conclude that EDRF may participate in the renal hemodynamic response to amino acid infusion.

Original languageEnglish
Pages (from-to)1045-1051
Number of pages7
JournalHypertension
Volume17
Issue number6 SUPPL. 2
StatePublished - Jun 1 1990
Externally publishedYes

Fingerprint

Endothelium-Dependent Relaxing Factors
Renal Plasma Flow
Glomerular Filtration Rate
Hemodynamics
Kidney
Amino Acids
Intravenous Infusions
Vasodilation
Blood Pressure
omega-N-Methylarginine
Angiotensin Receptor Antagonists
Phenylephrine
Angiotensin II
Blood Vessels
Arginine
Arterial Pressure
Nitric Oxide
Eating
Proteins

Keywords

  • Amino acids
  • Blood flow
  • Endothelium
  • Glomerular filtration rate
  • Hemodynamics
  • Nitric oxide

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Effects of amino acid infusion on renal hemodynamics role of endothelium-derived relaxing factor. / Tolins, Jonathan P.; Raij, Leopoldo.

In: Hypertension, Vol. 17, No. 6 SUPPL. 2, 01.06.1990, p. 1045-1051.

Research output: Contribution to journalArticle

Tolins, JP & Raij, L 1990, 'Effects of amino acid infusion on renal hemodynamics role of endothelium-derived relaxing factor', Hypertension, vol. 17, no. 6 SUPPL. 2, pp. 1045-1051.
Tolins, Jonathan P. ; Raij, Leopoldo. / Effects of amino acid infusion on renal hemodynamics role of endothelium-derived relaxing factor. In: Hypertension. 1990 ; Vol. 17, No. 6 SUPPL. 2. pp. 1045-1051.
@article{c523e743b3bd4549b0db0f1fd31cf19c,
title = "Effects of amino acid infusion on renal hemodynamics role of endothelium-derived relaxing factor",
abstract = "Ingestion of protein or intravenous infusion of amino acids acutely elevates glomerular filtration rate (GFR) and renal plasma flow (RPF) by unknown mechanisms. Endothelium-derived relaxing factor (EDRF), now known to be nitric oxide derived from metabolism of L-arginine, participates in local regulation of vascular tone. To investigate the hypothesis that EDRF may participate in the renal vasodilatation and increased GFR after amino acid infusion, we characterized the effect of inhibition of EDRF synthesis with NG-monomethyl L-arginine (LNMMA) on basal renal hemodynamics and the response to infusion of a 10{\%} mixed amino acid solution (1 ml/hr i.v.) in the rat. Renal arterial infusion of LNMMA (500 μg/kg/min) resulted in a significant increase in mean arterial pressure, decreases in GFR (20{\%}) and RPF (44{\%}), and a significant increase in filtration fraction. Pretreatment with the angiotensin II receptor antagonist Sar-Gly-angiotensin II did not prevent the increase in blood pressure but blunted the decreases in GFR (11{\%}) and RPF (27{\%}) after LNMMA infusion. Amino acid infusion in the untreated, fasted rat resulted in no change in blood pressure but significant increases in GFR and RPF; these effects were completely inhibited by intrarenal LNMMA but not an equihypertensive intravenous infusion of phenylephrine. In summary, EDRF participates in regulation of basal renal hemodynamics. Furthermore, amino acid-induced hyperfiltration and renal vasodilatation are completely prevented by inhibition of EDRF synthesis. We conclude that EDRF may participate in the renal hemodynamic response to amino acid infusion.",
keywords = "Amino acids, Blood flow, Endothelium, Glomerular filtration rate, Hemodynamics, Nitric oxide",
author = "Tolins, {Jonathan P.} and Leopoldo Raij",
year = "1990",
month = "6",
day = "1",
language = "English",
volume = "17",
pages = "1045--1051",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "6 SUPPL. 2",

}

TY - JOUR

T1 - Effects of amino acid infusion on renal hemodynamics role of endothelium-derived relaxing factor

AU - Tolins, Jonathan P.

AU - Raij, Leopoldo

PY - 1990/6/1

Y1 - 1990/6/1

N2 - Ingestion of protein or intravenous infusion of amino acids acutely elevates glomerular filtration rate (GFR) and renal plasma flow (RPF) by unknown mechanisms. Endothelium-derived relaxing factor (EDRF), now known to be nitric oxide derived from metabolism of L-arginine, participates in local regulation of vascular tone. To investigate the hypothesis that EDRF may participate in the renal vasodilatation and increased GFR after amino acid infusion, we characterized the effect of inhibition of EDRF synthesis with NG-monomethyl L-arginine (LNMMA) on basal renal hemodynamics and the response to infusion of a 10% mixed amino acid solution (1 ml/hr i.v.) in the rat. Renal arterial infusion of LNMMA (500 μg/kg/min) resulted in a significant increase in mean arterial pressure, decreases in GFR (20%) and RPF (44%), and a significant increase in filtration fraction. Pretreatment with the angiotensin II receptor antagonist Sar-Gly-angiotensin II did not prevent the increase in blood pressure but blunted the decreases in GFR (11%) and RPF (27%) after LNMMA infusion. Amino acid infusion in the untreated, fasted rat resulted in no change in blood pressure but significant increases in GFR and RPF; these effects were completely inhibited by intrarenal LNMMA but not an equihypertensive intravenous infusion of phenylephrine. In summary, EDRF participates in regulation of basal renal hemodynamics. Furthermore, amino acid-induced hyperfiltration and renal vasodilatation are completely prevented by inhibition of EDRF synthesis. We conclude that EDRF may participate in the renal hemodynamic response to amino acid infusion.

AB - Ingestion of protein or intravenous infusion of amino acids acutely elevates glomerular filtration rate (GFR) and renal plasma flow (RPF) by unknown mechanisms. Endothelium-derived relaxing factor (EDRF), now known to be nitric oxide derived from metabolism of L-arginine, participates in local regulation of vascular tone. To investigate the hypothesis that EDRF may participate in the renal vasodilatation and increased GFR after amino acid infusion, we characterized the effect of inhibition of EDRF synthesis with NG-monomethyl L-arginine (LNMMA) on basal renal hemodynamics and the response to infusion of a 10% mixed amino acid solution (1 ml/hr i.v.) in the rat. Renal arterial infusion of LNMMA (500 μg/kg/min) resulted in a significant increase in mean arterial pressure, decreases in GFR (20%) and RPF (44%), and a significant increase in filtration fraction. Pretreatment with the angiotensin II receptor antagonist Sar-Gly-angiotensin II did not prevent the increase in blood pressure but blunted the decreases in GFR (11%) and RPF (27%) after LNMMA infusion. Amino acid infusion in the untreated, fasted rat resulted in no change in blood pressure but significant increases in GFR and RPF; these effects were completely inhibited by intrarenal LNMMA but not an equihypertensive intravenous infusion of phenylephrine. In summary, EDRF participates in regulation of basal renal hemodynamics. Furthermore, amino acid-induced hyperfiltration and renal vasodilatation are completely prevented by inhibition of EDRF synthesis. We conclude that EDRF may participate in the renal hemodynamic response to amino acid infusion.

KW - Amino acids

KW - Blood flow

KW - Endothelium

KW - Glomerular filtration rate

KW - Hemodynamics

KW - Nitric oxide

UR - http://www.scopus.com/inward/record.url?scp=0026017879&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026017879&partnerID=8YFLogxK

M3 - Article

C2 - 2045148

AN - SCOPUS:0026017879

VL - 17

SP - 1045

EP - 1051

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 6 SUPPL. 2

ER -