August 1993
Volume 34, Issue 9
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Articles  |   August 1993
Prejunctional modulation of norepinephrine release in the human iris-ciliary body.
Author Affiliations
  • J E Jumblatt
    Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Research Institute, Univ. of Louisville School of Medicine.
  • S E Ohia
    Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Research Institute, Univ. of Louisville School of Medicine.
  • R C Hackmiller
    Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Research Institute, Univ. of Louisville School of Medicine.
Investigative Ophthalmology & Visual Science August 1993, Vol.34, 2790-2793. doi:
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    • Get Citation

      J E Jumblatt, S E Ohia, R C Hackmiller; Prejunctional modulation of norepinephrine release in the human iris-ciliary body.. Invest. Ophthalmol. Vis. Sci. 1993;34(9):2790-2793.

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

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Abstract

PURPOSE: To characterize the prejunctional mechanisms that control the impulse-evoked release of norepinephrine in the isolated, superfused human iris-ciliary body. METHODS: Human iris-ciliary body tissue segments were preincubated with 3H-norepinephrine, superfused and electrically-stimulated in vitro to evoke the discharge of 3H-norepinephrine. The effects of prejunctional modulators on evoked 3H-norepinephrine overflow were evaluated. RESULTS: Stimulation-evoked (but not spontaneous) 3H-norepinephrine release was inhibited by alpha 2-adrenergic, muscarinic, dopaminergic, neuropeptide Y, and prostaglandin agonists and was enhanced by angiotensin II. Agonist-induced effects on 3H-norepinephrine overflow were blocked by selective antagonists, where available. Yohimbine and atropine alone enhanced 3H-norepinephrine output, suggesting that prejunctional alpha 2-adrenergic and muscarinic receptors undergo tonic activation by endogenously released neurotransmitters. CONCLUSIONS: Human ocular sympathetic nerves express inhibitory alpha 2-adrenergic, muscarinic, dopaminergic, prostaglandin, and neuropeptide Y receptors and facilitatory angiotensin II receptors that control the impulse-evoked release of 3H-norepinephrine. These receptors may be useful targets for pharmacologic manipulation of the adrenergic system in vivo.

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