Transmitter Release and Uptake

Ascorbic acid stimulates the release of acetylcholine and noradrenaline from isolated synaptic vesicles (Kuo et aL, 1979). The release mechanisms of acetylcholine are more sensitive to ascorbic acid than those of noradrenaline (2-2.5 jlM vs. 20 xM of EC50 for ascorbic acid). Ascorbic acid also enhances the release of vasoactive intestinal polypeptide from neuroblastoma (Brick et aL, 1985) and that of luteinizing hormone-releasing hormone (LHRH) from the mediobasal hypothalamus in vitro (Miller and Cicero, 1986). The latter effect may not be due to the reductive property of ascorbic acid, since another reducing agent, sodium metabisulfite, did not induce the release of LHRH. 

Ascorbic acid modulates the secretion and mRNA expression of atrial natriure- 

Astrocytes take up noradrenaline by a temperature-dependent, sodium-independent mechanism that is saturable. This uptake of noradrenaline is inhibited by low concentrations of ascorbic acid (IC50 = 340 nM, Paterson and Hertz, 1989). Indeed, ascorbic acid deficiency leads to faster turnover of guinea pig brain noradrenaline (Saner et aL, 1975). 

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