May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Exogenous Arginine Vasopressin Increases Tear Fluid Secretion Via Vasopressin V1a Receptors in Rats
Author Affiliations & Notes
  • T. Kurasawa
    Sagami Research Laboratories, Wakamoto Pharmaceutical Co., Ltd., Ashigarakami–gun, Japan
  • A. Naito
    Sagami Research Laboratories, Wakamoto Pharmaceutical Co., Ltd., Ashigarakami–gun, Japan
  • Y. Ohtake
    Sagami Research Laboratories, Wakamoto Pharmaceutical Co., Ltd., Ashigarakami–gun, Japan
  • E. Shirasawa
    Sagami Research Laboratories, Wakamoto Pharmaceutical Co., Ltd., Ashigarakami–gun, Japan
  • Footnotes
    Commercial Relationships  T. Kurasawa, Wakamoto Pharmaceutical Co., Ltd. E; A. Naito, Wakamoto Pharmaceutical Co., Ltd. E; Y. Ohtake, Wakamoto Pharmaceutical Co., Ltd. E; E. Shirasawa, Wakamoto Pharmaceutical Co., Ltd. E.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 4407. doi:
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      T. Kurasawa, A. Naito, Y. Ohtake, E. Shirasawa; Exogenous Arginine Vasopressin Increases Tear Fluid Secretion Via Vasopressin V1a Receptors in Rats . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4407.

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

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Abstract

Abstract: : Purpose:The antidiuretic hormone, Arginine vasopressin (AVP), plays an important role in systemic homeostasis by regulating body fluid osmolarity and blood pressure. Also, AVP affects intraocular pressure and pupil size. However, its role in mediating regulation of tear flow has not been clarified. Accordingly, we evaluated the effect of AVP on tear fluid secretion in Crj:CD (SD) IGS rats and identified the receptor subtype eliciting this response. Methods: Tear fluid secretion in rats was measured with cotton threads 5min after intravenous administration of AVP (0.08–0.4 µg/kg) and [Phe2, Ile3, Orn8]vasopressin (V1 agonist, 0.4–1.6 µg/kg) under general anesthesia with pentobarbital sodium (40 mg/kg, i.p.). After intravenous administration of either SR49059 (selective V1a receptor antagonist, 0.1 mg/kg), SR–121463A (selective V2 receptor antagonist, 1 mg/kg), prazosin (alpha1–adrenergic receptor antagonist, 1 mg/kg), timolol (non–selective beta–adrenergic receptor antagonist, 1 mg/kg) or atropine (muscarinic receptor antagonist, 1mg/kg), AVP was injected intravenously and changes in the tear outflow were measured to delineate the specific receptor subtypes activated by AVP, which affect tear secretion. Results: AVP and [Phe2, Ile3, Orn8]vasopressin injections mediated dose dependent increases in tear outflow. Such increases were completely blocked by the pretreatment with SR49059. On the other hand, neither SR–121463A, prazosin, timolol nor atropine affected AVP–induced increases in tear secretion. Conclusions: These findings suggest that in rats exogenous AVP increases tear fluid secretion and this effect is mediated by vasopressin V1a receptors, rather than vasopressin V2, adrenergic or cholinergic receptors. Therefore, the development of novel selective V1a agonists could provide an effective means to treat dry eye symptomology in a clinical setting.

Keywords: cornea: tears/tear film/dry eye • neuropeptides • receptors: pharmacology/physiology 
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