Arterial vasodilatation in cirrhosis: Role of the L-arginine transporter system

Norfloxacin treatment for clinically significant portal hypertension: results of a randomised double‐blind placebo‐controlled crossover trial

“…Endotoxaemia was not detected in any of the subjects and NO x did not vary with treatment. The rate of L-Arg transport in cirrhotic subjects was similar to that noted previously (15). As shown in Figure 3, no significant difference was detected in L-Arg transport after treatment with norfloxacin compared with placebo.…”

“…The increased production of NO in the systemic and splanchnic circulation of cirrhosis could therefore be in part accounted for by increased L-Arg transport. This hypothesis is supported by the findings of upregulation of the L-Arg transporter, cationic amino acid transporter (CAT), in subjects with chronic liver disease (15) and by data obtained in other disease models (16)(17)(18).…”

“…Cellular uptake of L-Arg is controlled by the CATs, which provide NOS with the necessary substrate L-Arg for NO synthesis. LPS can induce CATs (31) and, furthermore, the L-Arg transporter system is upregulated in cirrhosis (15) and hence may contribute to the increased systemic NO observed in this condition. We found no difference in the functioning of the L-Arg transporter with norfloxacin therapy, indicating that there are likely alternative mechanisms for the alteration of NO production by norfloxacin.…”