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.
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)