June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Role of adrenergic stimulation on lacrimal gland ductal fluid secretion in mice
Author Affiliations & Notes
  • Orsolya Berczeli
    Department of Ophthalmology, University of Szeged, Szeged, Hungary
  • Vizvari Eszter
    Department of Ophthalmology, University of Szeged, Szeged, Hungary
  • Mate Katona
    First Department of Internal Medicine, University of Szeged, Szeged, Hungary
  • Zoltan Rakonczay
    First Department of Internal Medicine, University of Szeged, Szeged, Hungary
    Department of Pathophysiology, University of Szeged, Szeged, Hungary
  • Peter Hegyi
    First Department of Internal Medicine, University of Szeged, Szeged, Hungary
  • Chuanqing Ding
    Pharmacology and Pharmaceutic Sciences, Ophthalmology, University of Southern California, Los Angeles, California, United States
  • Edit Toth-Molnar
    Department of Ophthalmology, University of Szeged, Szeged, Hungary
    Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary
  • Footnotes
    Commercial Relationships   Orsolya Berczeli, None; Vizvari Eszter, None; Mate Katona, None; Zoltan Rakonczay, None; Peter Hegyi, None; Chuanqing Ding, None; Edit Toth-Molnar, None
  • Footnotes
    Support  NKFIH NN 115611; The Webb Foundation Grant; NIH/NEI-R01 EY017731, HARVO Travel Grant
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 2256. doi:
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      Orsolya Berczeli, Vizvari Eszter, Mate Katona, Zoltan Rakonczay, Peter Hegyi, Chuanqing Ding, Edit Toth-Molnar; Role of adrenergic stimulation on lacrimal gland ductal fluid secretion in mice. Invest. Ophthalmol. Vis. Sci. 2017;58(8):2256.

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

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Abstract

Purpose : Earlier reports demonstrated that both α and β adrenergic agonists could stimulate secretory response in whole lacrimal gland (LG) pieces in mouse, suggesting the direct role of adrenergic system in LG secretion. However, whether their effects are through acinar cells or ductal cells remained unknown. Therefore the aim of the present study was to investigate the effect of adrenergic stimulation on fluid secretion of isolated LG duct segments in mouse.

Methods : Interlobular and intralobar ducts were isolated from mouse LG as previously described by us. During incubation, ends of the ducts seal forming a closed intraluminal space. Fluid secretion into the lumen results in swelling of the ducts. This response was analyzed using video-microscopy. Secretory effects of α1-adrenergic agonist phenylephrine (10 µM, in the presence of β-antagonist [1 µM propranolol]), β-adrenergic agonist isoproterenol (100 µM, in the presence of α-antagonist [10 µM phentolamine]) and the effect of norepinephrine (10 µM) were investigated. This latter transmitter can stimulate both α- and β- receptors. Data was presented as means ± SEM.

Results : Phenylephrine stimulation caused a rapid fluid secretory response (secretory rate in the first 10 min of stimulation: 187.8±26.8 pl/min/mm2) in the isolated duct segments. Isoproterenol failed to elicit any detectable secretory effect (secretory rate: -0.8±19.7 pl/min/mm2) while norepinephrine initiated a rapid response (189.6±13.9 pl/min/mm2 in the first 10 min of stimulation). We could not detect statistically significant difference between the fluid secretory rates evoked by phenylephrine and norepinephrine (p=0.42) and the kinetics of secretion was also similar.

Conclusions : These data suggest the direct role of α adrenergic stimulation in LG ductal fluid secretion. Lack of isoproterenol-induced fluid secretory response suggests the absence of β-receptor mediated pathway in mouse LG ducts. The similar secretory effects of norepinephrine and phenylephrine suggest that α-adrenergic stimulation may be the dominant adrenergic pathway in mouse LG ducts. Considering the robust response observed, sympathetic innervation may have more functional significance than previously believed.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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