Ethanol inhibits L-arginine uptake and enhances NO formation in human placenta

The acute effects of ethanol (20 - 60 mM) on L-arginine uptake and nitric oxide (NO) formation was investigated in human placental cotyledons perfused at constant flow. Ethanol (40 mM) decreased L-[³H]arginine uptake from 27.6 ± 2.3 to 15.8 ± 1.3 per cent (P< 0.05) of the injected dose and significantly enhanced NO levels in the perfusate from 0.88 ± 0.11 to 2.80 ± 0.39 μM. Ethanol also elicited the constriction of placental vessels. The effects of ethanol (20 - 60 mM) on L-arginine uptake and endothelial NO synthase (eNOS) activity were also investigated in cultured human umbilical vein endothelial cells (HUVEC). After 60 min of ethanol (40 mM) exposure, basal L-[³H]arginine uptake (4.7 ± 0.3 pmol/μg protein/min) was inhibited by 60 per cent (P< 0.05). Basal eNOS activity in HUVEC determined under "no flow" (static) conditions was significantly increased (∼ 1.8 fold) by 60 mM ethanol. These data are consistent with a stimulatory effect of ethanol on eNOS activity in both basal and flow-stimulated conditions, which may serve a protective role against its vasoconstrictive acute effect. While acute ethanol administration inhibits L-arginine uptake, the present results do not allow us to speculate on the effects of chronic ethanol exposure on NO formation in the fetoplacental unity.