Arginine transport in human liver. Characterization and effects of nitric oxide synthase inhibitors.

@article{Inoue1993ArginineTI,
  title={Arginine transport in human liver. Characterization and effects of nitric oxide synthase inhibitors.},
  author={Y. Inoue and B. Bode and D. Beck and A. Li and K. Bland and W. Souba},
  journal={Annals of surgery},
  year={1993},
  volume={218 3},
  pages={
          350-62; discussion 362-3
        }
}
OBJECTIVE Arginine transport was characterized and studied in human liver. SUMMARY BACKGROUND DATA Plasma arginine uptake may regulate hepatocyte intracellular availability and the subsequent biosynthesis of nitric oxide (NO), but little is known about arginine transport across the human hepatocyte plasma membrane. METHODS The authors characterized plasma membrane transport of 3[H]-L-arginine in hepatic plasma membrane vesicles (HPMVs) and in hepatocytes isolated and cultured from human… Expand
Characterization of L-arginine transporters in rat renal inner medullary collecting duct.
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TLDR
Results indicate that L-arginine uptake by IMCD cells occurs via system y(+), is encoded by CAT1, and may participate in the regulation of NO production in this renal segment, supporting the important role of L- arginine transport for NO production by this tubular segment. Expand
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In vivo treatment with TNF results in a rapid stimulation of saturable, System y(+)-mediated arginine transport in the liver, which may serve to increase the normally restricted availability of extrahepaticArginine to the hepatocyte intracellular space during a septic insult to support important arginin-dependent pathways in the Liver. Expand
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Data indicate that the accelerated hepatic alanine consumption which occurs during endotoxemia is primarily the result of increased hepatic substrate delivery, and that delivery begins to outdistance the metabolic capacity of the hepatocyte to utilizeAlanine and intracellular alAnine levels rise. Expand
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The transport of L-arginine by porcine pulmonary artery endothelial cells (PAECs) was characterized and Na(+)-dependent arginine uptake was pH and hormone insensitive, and lithium did not substitute effectively for sodium. Expand
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The marked increase in Na(+)-dependent amino acid transport activity by TNF is mediated in part by the glucocorticoid hormones and represents an important mechanism underlying the accelerated hepatic amino acid uptake that occurs during critical illness. Expand
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TLDR
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TLDR
No single cytokine, but rather a specific combination of tumor necrosis factor, interleukin-1, interferon-gamma, and endotoxin, were required for maximal induction of HC nitrogen oxide production. Expand
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