April 1997
Volume 38, Issue 5
Free
Articles  |   April 1997
Regulation of uveal sympathetic neurotransmission by peroxides.
Author Affiliations
  • C Opere
    Department of Pharmaceutical and Administrative Sciences, Creignton University Health Sciences Center, Omaha, Nebraska 68178, USA.
  • L Tang
    Department of Pharmaceutical and Administrative Sciences, Creignton University Health Sciences Center, Omaha, Nebraska 68178, USA.
  • M Imler
    Department of Pharmaceutical and Administrative Sciences, Creignton University Health Sciences Center, Omaha, Nebraska 68178, USA.
  • J Kim
    Department of Pharmaceutical and Administrative Sciences, Creignton University Health Sciences Center, Omaha, Nebraska 68178, USA.
  • M Okoye, Jr
    Department of Pharmaceutical and Administrative Sciences, Creignton University Health Sciences Center, Omaha, Nebraska 68178, USA.
  • S Ohia
    Department of Pharmaceutical and Administrative Sciences, Creignton University Health Sciences Center, Omaha, Nebraska 68178, USA.
Investigative Ophthalmology & Visual Science April 1997, Vol.38, 842-847. doi:
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    • Get Citation

      C Opere, L Tang, M Imler, J Kim, M Okoye, S Ohia; Regulation of uveal sympathetic neurotransmission by peroxides.. Invest. Ophthalmol. Vis. Sci. 1997;38(5):842-847.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: To investigate the effect of naturally occurring and synthetic peroxides on norepinephrine release from isolated iris-ciliary bodies of several mammalian species. METHODS: Hemiirides (bovine) and iris-ciliary bodies (human, rabbit, and rat) were incubated in Krebs solution containing [3H]-norepinephrine ([3H]NE) for 60 minutes. After incubation, tissues were set up for studies of [3H]NE release using the superfusion method. Release of [3H]NE was elicited through electrical field stimulation. RESULTS: In bovine irides, hydrogen peroxide (H2O2), cumene hydroperoxide (cuOOH), and tert-butyl hydroperoxide (buOOH) caused a concentration-dependent potentiation of field-stimulated [3H]NE release with the following rank order of potency: cuOOH > H2O2 > buOOH. Furthermore, the free radical scavenger, melatonin (2 mM), prevented the enhancement of evoked [3H]NE overflow elicited by H2O2 and cuOOH. At equimolar concentrations, H2O2 (1 mM) increased stimulated [3H]NE release from rabbit, human (mean age, 29.7; range, 15 to 48 years), and Fischer 344 rat (4 months old) iris-ciliary bodies by 98%, 50%, and 40%, respectively. However, H2O2 (1 mM) caused a 9% increase in evoked [3H]NE release in tissue from aged Fischer 344 rats (30 months old) and a 5% decrease in neurotransmitter release in tissue from old human donors (mean age, 72.3 years; range, 69 to 74 years). CONCLUSIONS: Peroxides such as H2O2 can potentiate sympathetic neurotransmission in the anterior uvea of several mammalian species. In bovine irides, H2O2-induced enhancement of neurotransmitter release can be mimicked by synthetic peroxides and may involve the generation of reactive oxygen species.

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