Endothelin Modulation of Choroidal Blood Flow in the Rabbit

Kiel, Jeffrey W.

doi:10.1006/exer.2000.0911

Cited by 71 publications

(59 citation statements)

References 19 publications

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“…[22][23][24] Some of the proposed vasoregulatory mechanisms are the nitric oxide, endothelins, and the autonomic nervous system. [25][26][27] However, such mechanisms appear to be incomplete and labile. The choriocapillaris oxygen partial pressure is so high that it seems likely that the choroidal circulation is regulated by additional factors different from those acting in other vascular beds.…”

Section: Discussionmentioning

confidence: 99%

Choroidal Thickness in Nonarteritic Anterior Ischaemic Optic Neuropathy: A Study with Optical Coherence Tomography

Dias‐Santos

Ferreira

Pinto

et al. 2014

Neuro-Ophthalmology

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Nonarteritic anterior ischemic optic neuropathy (NA-AION) is the most common nonglaucomatous optic neuropathy in adults over 50 years of age. It is usually related to cardiovascular risk factors. The primary objective of this study was to evaluate choroidal thickness in patients with chronic NA-AION, and the secondary objective was to evaluate macular thickness in these patients. This cross-sectional study compared two groups: group 1 included 20 eyes of 20 patients with chronic NA-AION, and group 2 included 31 eyes of 31 healthy controls. In both groups, the choroidal thickness was measured using the enhanced depth imaging program of Heidelberg Spectralis Õ optical coherence tomography (Heidelberg Engineering, Heidelberg, Germany). The macular thickness was also measured using the automatic software of the same device. The mean follow-up time after NA-AION in group 1 was 57.17 ± 26.92 months. The mean choroidal thickness of the posterior pole was 244.38 ± 61.03 mm in group 1 and 214.18 ± 65.97 mm in group 2 (p = 0.004). The mean macular thickness was higher in group 2. Macular thickness is reduced in eyes that had an episode of NA-AION, whereas choroidal thickness is generally higher in these eyes when compared with normal eyes. The increase in choroidal thickness may be due to a local dysfunction in vascular autoregulatory mechanisms, which may predispose to ischemic phenomena.

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Section: Discussionmentioning

confidence: 99%

Choroidal Thickness in Nonarteritic Anterior Ischaemic Optic Neuropathy: A Study with Optical Coherence Tomography

Dias‐Santos

Ferreira

Pinto

et al. 2014

Neuro-Ophthalmology

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“…[2][3][4][5] Activation of ET A receptors in the ocular vascular systems induces strong vasoconstriction, whereas stimulation of ET B receptors leads to vasodilation through the formation of nitric oxide (NO). 6 Despite extensive studies on the effects induced by ET-1 on the vascular system including retinal and optic nerve head circulation, the precise roles of ET-1 on neurotransmission and neuronal damage in the retina remain to be clarified.…”

Section: ϫ10mentioning

confidence: 99%

Endothelin-1 Enhances Glutamate-Induced Retinal Cell Death, Possibly through ET_AReceptors

Kobayashi

Oku

Fukuhara

et al. 2005

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To determine the modification of the glutamate-induced death of retinal neurons by endothelin (ET)-1. METHODS. Cultured retinal neurons from fetal rats were exposed to glutamate (1.0 mM) alone or glutamate with ET-1 (10 Ϫ10-10 Ϫ7 M) for 10 minutes. Neuronal death was assessed by the trypan blue exclusion or TUNEL assays at 2, 6, and 24 hours after the exposure. The effects of adding BQ-123 or BQ-788, ET A , and ET B receptor antagonists, respectively, in combination with ET-1 was also assessed. RESULTS. Immunohistochemical analyses showed that the ETs as well as ET A and ET B receptors were expressed on cultured retinal neurons consisting mainly of amacrine cells. A brief exposure of the cultured retinal neurons to glutamate alone significantly increased the number of dead cells, and the addition of ET-1 with glutamate caused a further significant increase in retinal neuronal death compared with the cells exposed to glutamate alone. A significant increase in neuronal death was detected at doses of 10 nM of ET-1 and higher after a 24-hour exposure (P Ͻ 0.05, Dunnett), whereas brief exposure of neurons to up to 1 M ET-1 alone did not cause delayed cell death of neurons. BQ-123 (10 nM) suppressed the enhancement of retinal toxicity caused by ET-1 (10 nM), whereas BQ-788 had no significant effect. CONCLUSIONS. These results indicate that ET-1 enhances glutamate-induced retinal cell death, possibly through ET A receptors. ET-1 may act synergistically with glutamate to damage retinal neurons under hypoxic conditions. (Invest Ophthalmol Vis Sci. 2005;46:4684 -4690)

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“…ophthalmic artery (Flammer & Lu¨s-cher 1992 and in the ophthalmic and ciliary arteries of the pig (Haefliger et al 1993). Its intra-arterial administration in humans or animals has resulted in a significant reduction of blood flow through the retina, choroid and optic nerve head (Schmetterer et al 1997;Dallinger et al 2000;Kiel 2000).…”

Section: Discussionmentioning

confidence: 99%

“…ET-1 and its receptors are present in the choroid (Stitt et al 1996); however, there are relatively few studies on their haemodynamic effects. According to Kiel (2000) in anaesthetized rabbits the choroid has a biphasic response to ET-1, as seen in other tissues (i.e. initial brief dilation followed by prolonged vasoconstriction).…”

Section: Introductionmentioning

confidence: 98%

Endothelin‐1 effects on spontaneous oscillations in choroidal arterioles

Delgado¹,

Marques-Neves²,

Rocha³

et al. 2009

Acta Ophthalmologica

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ABSTRACT.Purpose: This study characterizes the effects of endothelin-1 (ET-1) on the perfusion pressure of the choroidal vasculature using in situ perfused isolated rabbit eyes. Methods: Rabbit external ophthalmic arteries (n = 12) in a head-mounted preparation were cannulated and perfused with warmed tyrode. The three-way polypropylene catheter was further connected to a pressure transducer and the effect of intraluminal pressure as a measure of total vascular resistance was assessed. Response curves to intra-arterial injections of ET-1 (group A; n = 6) and to an intravitreal injection followed by an intra-arterial injection of ET-1 (group B; n = 6) were obtained. Data were studied using paired t-test and fast Fourier transform. Results: Before any drugs were administered, spontaneous oscillations were observed in the 12 rabbit models. In group A, ET-1 induced a short and weak vasodilating effect followed by a strong and long-lasting vasoconstrictor tone. Vasomotion became more evident, showing a higher frequency and shorter amplitude of oscillations. In group, B the intravitreal injection produced no significant changes in registered pressure or vasomotion characteristics. The intra-arterial injection produced effects similar to those observed in group A. Conclusion: Our study has three main findings: (i) the choroidal vasculature demonstrated spontaneous oscillations in perfusion pressure in basal conditions in all rabbit eye models; (ii) ET-1 applied intra-arterially induced a short drop in perfusion pressure followed by a long withstanding contraction; and (iii) intra-arterial ET-1 modulated the frequency and amplitude of the spontaneous oscillations, causing a faster rate of pulsatility.

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Endothelin Modulation of Choroidal Blood Flow in the Rabbit

Cited by 71 publications

References 19 publications

Choroidal Thickness in Nonarteritic Anterior Ischaemic Optic Neuropathy: A Study with Optical Coherence Tomography

Choroidal Thickness in Nonarteritic Anterior Ischaemic Optic Neuropathy: A Study with Optical Coherence Tomography

Endothelin-1 Enhances Glutamate-Induced Retinal Cell Death, Possibly through ET_AReceptors

Endothelin‐1 effects on spontaneous oscillations in choroidal arterioles

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Endothelin Modulation of Choroidal Blood Flow in the Rabbit

Cited by 71 publications

References 19 publications

Choroidal Thickness in Nonarteritic Anterior Ischaemic Optic Neuropathy: A Study with Optical Coherence Tomography

Choroidal Thickness in Nonarteritic Anterior Ischaemic Optic Neuropathy: A Study with Optical Coherence Tomography

Endothelin-1 Enhances Glutamate-Induced Retinal Cell Death, Possibly through ETAReceptors

Endothelin‐1 effects on spontaneous oscillations in choroidal arterioles

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Endothelin-1 Enhances Glutamate-Induced Retinal Cell Death, Possibly through ET_AReceptors