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Exogenous L‐Arginine (L‐Arg) attenuates the vasoconstrictor response to Angiotensin II (Ang II) stimulation in isolated rat aortic rings
Author(s) -
Das Satarupa,
Mattson David L
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.665.9
Subject(s) - angiotensin ii , contraction (grammar) , chemistry , vasoconstriction , medicine , endocrinology , phenylephrine , arginine , stimulation , nitric oxide , nitric oxide synthase , amino acid , biochemistry , blood pressure
Previous studies demonstrated that infusion of AngII (20 ng/kg/min iv) in rats significantly reduces renal blood flow (RBF) and glomerular filtration rate (GFR) by 27% and 42%, respectively. Co‐administration of exogenous L‐Arg (300 ìg/kg/min) attenuates Ang II mediated reductions in GFR and RBF. The present study examined mechanisms by which L‐Arg modulates AngII induced vasoconstriction in isolated aortic rings from male Sprague Dawley rats (n=6–8/group). Dose‐dependent contraction to Ang II (10‐10M to 10‐6M) was observed with a maximal force of contraction equal to 27±3% of the maximal response to 10‐5M phenylephrine. Contraction to 10‐7M Ang II was significantly blunted by 75±3% with 10‐4M L‐Arg. The influence of L‐Arg to blunt Ang II mediated contraction was eliminated by endothelial denudation or incubation with the nitric oxide synthase inhibitors L‐NAME (10‐4M ) or LNMMA (10‐4M ). L‐Arg's effects were eliminated by addition of 10‐4M cationic (L‐Orn, L‐Lys, L‐HArg) or neutral amino acids (L‐Ser, L‐Thr) which interfere with cellular L‐Arg uptake. The anionic amino acids L‐Asp or L‐Glu did not influence L‐Arg effects on AngII‐mediated contraction. The present studies demonstrate that L‐Arg blunts AngII‐mediated vascular contraction by an endothelial‐ and NOS‐dependent mechanism that involves cellular uptake of L‐Arg via y+ or y+L transporters. Supported by HL29587 and DK062803.