E L Gondim1, J H Liu, V P Costa, R N Weinreb. 1. Glaucoma Center, Department of Ophthalmology, University of California-San Diego, La Jolla, CA 92093-0946, USA.
Abstract
PURPOSE: To compare central, peripheral, and ocular effects of exogenously given vasopressin on intraocular pressure (IOP) and to identify the related receptor mechanisms of action in rabbits. METHODS: Young adult New Zealand albino rabbits were entrained under a daily 12-hour light and 12-hour dark cycle. In the early light period, bolus injections of vasopressin or desmopressin (a specific V(2) receptor agonist) were given either to the central nervous system (CNS) through an implanted cannula to the 3(rd) ventricle or to the systemic circulation via the ear vein in conscious rabbits. Changes in IOP and pupil size were monitored for up to 6 hours and dose-response curves were generated. Effects of centrally and peripherally given vasopressin on IOP were further examined following pretreatments with a selective V(1) receptor antagonist administered into the 3(rd) ventricle and into the ear vein, respectively. In order to clarify whether or not exogenously given vasopressin can alter IOP by mechanisms inside the eye, vasopressin was injected into the anterior chamber or the vitreous chamber unilaterally in conscious rabbits. Changes in IOP and pupil size were monitored. After an anterior chamber or intravitreal injection of the V(1) receptor antagonist, changes in IOP and pupil size due to an intravenous injection of vasopressin were determined to study the involvement of the related receptor mechanism. RESULTS: A dose-dependent elevation of IOP appeared after injections of vasopressin into the 3(rd) ventricle. There was no pupillary change. This IOP elevation was blocked by the pretreatment with the V(1) receptor antagonist. Following intravenous injections of vasopressin, significant reductions of IOP and pupil size occurred. These reductions were blocked by the pretreatment with the V(1) receptor antagonist. Intracerebroventricular or intravenous injection of desmopressin had no effect on IOP or pupil size. Injection of vasopressin into the anterior chamber or the vitreous chamber caused significant reductions of IOP and pupil size. Pretreatment with the V(1) receptor antagonist into the anterior chamber or the vitreous chamber prevented the reductions of IOP and pupil size following an intravenous injection of vasopressin. CONCLUSIONS: Intracerebroventricular and intravenous injections of vasopressin cause opposite effects on IOP. The central effect of vasopressin on IOP and the peripheral effects of vasopressin on IOP and pupil size are due to stimulations of the V(1) receptors. Reductions of IOP and pupil size following intravenous injections of vasopressin are at least partially due to stimulations of the V(1) receptors inside the eye.
PURPOSE: To compare central, peripheral, and ocular effects of exogenously given vasopressin on intraocular pressure (IOP) and to identify the related receptor mechanisms of action in rabbits. METHODS: Young adult New Zealand albino rabbits were entrained under a daily 12-hour light and 12-hour dark cycle. In the early light period, bolus injections of vasopressin or desmopressin (a specific V(2) receptor agonist) were given either to the central nervous system (CNS) through an implanted cannula to the 3(rd) ventricle or to the systemic circulation via the ear vein in conscious rabbits. Changes in IOP and pupil size were monitored for up to 6 hours and dose-response curves were generated. Effects of centrally and peripherally given vasopressin on IOP were further examined following pretreatments with a selective V(1) receptor antagonist administered into the 3(rd) ventricle and into the ear vein, respectively. In order to clarify whether or not exogenously given vasopressin can alter IOP by mechanisms inside the eye, vasopressin was injected into the anterior chamber or the vitreous chamber unilaterally in conscious rabbits. Changes in IOP and pupil size were monitored. After an anterior chamber or intravitreal injection of the V(1) receptor antagonist, changes in IOP and pupil size due to an intravenous injection of vasopressin were determined to study the involvement of the related receptor mechanism. RESULTS: A dose-dependent elevation of IOP appeared after injections of vasopressin into the 3(rd) ventricle. There was no pupillary change. This IOP elevation was blocked by the pretreatment with the V(1) receptor antagonist. Following intravenous injections of vasopressin, significant reductions of IOP and pupil size occurred. These reductions were blocked by the pretreatment with the V(1) receptor antagonist. Intracerebroventricular or intravenous injection of desmopressin had no effect on IOP or pupil size. Injection of vasopressin into the anterior chamber or the vitreous chamber caused significant reductions of IOP and pupil size. Pretreatment with the V(1) receptor antagonist into the anterior chamber or the vitreous chamber prevented the reductions of IOP and pupil size following an intravenous injection of vasopressin. CONCLUSIONS: Intracerebroventricular and intravenous injections of vasopressin cause opposite effects on IOP. The central effect of vasopressin on IOP and the peripheral effects of vasopressin on IOP and pupil size are due to stimulations of the V(1) receptors. Reductions of IOP and pupil size following intravenous injections of vasopressin are at least partially due to stimulations of the V(1) receptors inside the eye.
Authors: Barbara Bogner; Birgit Tockner; Christian Runge; Clemens Strohmaier; Andrea Trost; Manuela Branka; Wolfgang Radner; Jeffrey W Kiel; Falk Schroedl; Herbert A Reitsamer Journal: Invest Ophthalmol Vis Sci Date: 2011-09-09 Impact factor: 4.799
Authors: Barbara Bogner; Christian Runge; Clemens Strohmaier; Andrea Trost; Birgit Tockner; Jeffrey W Kiel; Falk Schroedl; Herbert A Reitsamer Journal: Invest Ophthalmol Vis Sci Date: 2014-01-21 Impact factor: 4.799