Toxicological effects of ethanol on norepinephrine release and the response of the mammalian iris-ciliary body to pharmacological agents

There is evidence that chronic alcohol administration can impair pupillary function and response to light. The present study was conducted to establish whether in vivo or in vitro exposure of irides to ethanol could alter sympathetic neurotransmission and the response of the iris to pharmacological agents. The effect of chronic administration of ethanol on sympathetic neurotransmission in rats was examined by studying electrical field-stimulated release of ³H-norepinephrine ([³H]NE)from iris-ciliary bodies of ethanol-treated and ethanol-naive animals in vitro. Furthermore, we investigated the effect of medium to high concentrations of ethanol, applied in vitro, on evoked [³H]NE release from isolated rat, human, bovine and rabbit iris-ciliary bodies. The effect of ethanol was also studied on contractile and relaxant responses of bovine isolated irides to pharmacological agents. In vitro application of ethanol (100 mM) attenuated significantly, the overflow of [³H]NE from iris-ciliary body of rats on a chronic alcohol diet but had no effect on animals on an isocaloric control diet. Ethanol (300 mM) caused more than a five-fold increase in stimulated [³H]NE release from isolated human, rat, bovine and rabbit iris-ciliary bodies. In bovine isolated irides, ethanol (10-100 mM) caused a concentration-dependent attenuation of contractile responses to carbachol and pilocarpine, but had no effect on responses to PGF(2α) and potassium chloride. Although, ethanol (100 mM) attenuated relaxant responses of the bovine iris to isoproterenol, relaxations elicited by papaverine were unaffected by this agent. We conclude that ethanol selectively impairs both adrenergic neurosecretion in mammalian iris-ciliary bodies and postjunctional response of bovine irides to pharmacological agents.