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Intraocular pressure modulation by neuropeptides ‐ the effect of vasopressin
Author(s) -
BOGNER B,
RUNGE C,
STROHMAIER C,
TROST A,
KASEREICHBERGER A,
KREFFT K,
GRABNER G,
KIEL JW,
SCHROEDL F,
REITSAMER HA
Publication year - 2014
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2014.3431.x
Subject(s) - vasopressin , glaucoma , medicine , intraocular pressure , neuropeptide , ophthalmology , endocrinology , receptor
Elevated intraocular pressure (IOP) is a major risk factor for glaucoma. Currently, the primary strategy to slow down glaucoma progression is IOP reduction. Numerous studies investigated the IOP lowering effects of neuropeptides, but the complex physiological mechanisms involved are difficult to interpret. Therefore, we investigated the effect of arginine‐vasopressin (AVP) on IOP in a multiparameter approach. In a rabbit model the effect of i.v.‐applied AVP on IOP, ciliary blood flow (CilBF) and aqueous flow (AqF) was measured simultaneously by manometry, laser‐Doppler flowmetry and fluorophotometry. AVP caused a dose‐dependent decrease of IOP, CilBF and AqF. Based on the Goldmann equation the decrease of AqF at 0.08 ng/kg/min AVP (low dose) accounted for 77.1% of the IOP reduction (9.56±2.35%), while AqF at 1.33 ng/kg/min AVP (high dose) accounted for 28.4% of the IOP decline (41.02±3.19%). The results indicate that AqF reduction by low dose AVP is mainly caused by inhibition of ciliary epithelium secretion. At high dose AVP AqF reduction is caused by decreased CilBF or more likely by a combination of CilBF decline and secretory inhibition. This conclusion is only possible with the multiparameter measurement approach presented.