dc.creatorGondim, EL
dc.creatorLiu, JHK
dc.creatorCosta, VP
dc.creatorWeinreb, RN
dc.date2001
dc.date2014-07-30T17:32:01Z
dc.date2015-11-26T16:50:37Z
dc.date2014-07-30T17:32:01Z
dc.date2015-11-26T16:50:37Z
dc.date.accessioned2018-03-28T23:37:23Z
dc.date.available2018-03-28T23:37:23Z
dc.identifierCurrent Eye Research. Swets Zeitlinger Publishers, v. 22, n. 4, n. 295, n. 303, 2001.
dc.identifier0271-3683
dc.identifierWOS:000170203600008
dc.identifier10.1076/ceyr.22.4.295.5508
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/66312
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/66312
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1275771
dc.descriptionPurpose. 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.
dc.description22
dc.description4
dc.description295
dc.description303
dc.languageen
dc.publisherSwets Zeitlinger Publishers
dc.publisherLisse
dc.publisherHolanda
dc.relationCurrent Eye Research
dc.relationCurr. Eye Res.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectintraocular pressure
dc.subjectpupil
dc.subjectrabbit
dc.subjectvasopressin
dc.subjectV-1 receptor
dc.subjectArginine-vasopressin
dc.subjectIntracellular Calcium
dc.subjectConscious Rabbits
dc.subjectNucleus
dc.subjectStimulation
dc.subjectOxytocin
dc.subjectHormone
dc.titleExogenous vasopressin influences intraocular pressure via the V-1 receptors
dc.typeArtículos de revistas


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