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Arginine rapidly dilates intestinal microvessels and resistance arteries by increasing NO production
Author(s) -
Pezzuto Laura,
Bohlen Glenn
Publication year - 2006
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.20.4.a270-a
Subject(s) - arginine , vascular resistance , blood flow , medicine , microcirculation , endothelium , artery , blood vessel , endocrinology , chemistry , blood pressure , biochemistry , amino acid
To what extent the arginine is taken from intracellular stores or transported into the endothelial cell by the cationic amino acid transporter‐1for immediate use by eNOS is not known. To evaluate the rapidity of NO and vascular dilatory responses to exogenous arginine, individual in vivo arterioles or the entire vasculature was exposed to 100–400mM arginine. To evaluate artery versus microvascular resistance responses, blood flow and blood pressure in the largest arterioles was measured. The lowest arginine concentration to cause consistent dilation was 100 uM applied to the entire tissue. Dilatory responses to arginine by single arterioles began in 10‐15 seconds after release of 200 or 400 uM. Arginine applied to the entire vasculature caused increased blood flow and (NO) within 2 minutes and the response was fully developed by 4 minutes. The blood flow increased 19%, 32, and 50% with 100, 200, and 400 uM arginine. The reduction in arterial resistance during topical arginine was somewhat greater than the microvasculature at 100 and 200 uM arginine. The data indicate that rapid transport of arginine immediately influences NO production and vascular resistance of both intestinal resistance arteries and microvessels at arginine concentrations that could be produced through dietary supplementation of arginine. (Supported by NIH HL‐20605)