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Am J Physiol Lung Cell Mol Physiol 281: L1232-L1239, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 5, L1232-L1239, November 2001

Cytokine treatment increases arginine metabolism and uptake in bovine pulmonary arterial endothelial cells

Leif D. Nelin, Heather E. Nash, and Louis G. Chicoine

Vascular Physiology Group and Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131

L-Arginine (L-Arg) is metabolized to nitric oxide (NO) by NO synthase (NOS) or to urea by arginase (AR). L-Arg is transported into bovine pulmonary arterial endothelial cells (BPAECs) by cationic amino acid transporter-2 (CAT-2). We hypothesized that cytokine treatment would increase L-Arg metabolism and increase CAT-2 mRNA expression. BPAECs were incubated for 24 h in medium (control) or medium with lipopolysaccharide and tumor necrosis factor-alpha (L-T). L-T increased nitrite production (3.1 ± 0.4 nmol/24 h vs. 1.8 ± 0.1 nmol/24 h for control; P < 0.01) and urea production (83.5 ± 29.5 nmol/24 h vs. 17.8 ± 8.6 nmol/24 h for control; P < 0.05). L-T-treated BPAECs had greater endothelial and inducible NOS mRNA expression compared with control cells. Increasing the medium L-Arg concentration resulted in increased nitrite and urea production in both the control and the L-T-treated BPAECs. L-T treatment resulted in measurable CAT-2 mRNA. L-T increased L-[3H]Arg uptake (5.78 ± 0.41 pmol vs. 4.45 ± 0.10 pmol for control; P < 0.05). In summary, L-T treatment increased L-Arg metabolism to both NO and urea in BPAECs and resulted in increased levels of CAT-2 mRNA. This suggests that induction of NOS and/or AR is linked to induction of CAT-2 in BPAECs and may represent a mechanism for maintaining L-Arg availability to NOS and/or AR.

urea; cationic amino acid transport; tumor necrosis factor; lipopolysaccharide; nitric oxide synthase; arginase


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