Endothelin-Like Immunoreactivity in the Aqueous Humour and in Conditioned Medium from Cultured Ciliary Epithelial Cells

Lepple-Wienhues, Albrecht; Becker, Marion; Stahl, Frank; Berweck, S.; Hensen, J.; Noske, W; Eichhorn, Michael; Wiederholt, Michael

doi:10.3109/02713689209015075

Cited by 78 publications

(44 citation statements)

References 14 publications

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“…Endothelin-like immunoreactivity is 2–3 times higher in aqueous humor of human and bovine eyes than in the corresponding plasma [32, 56], and an elevation of endothelin-like immunoreactivity in the aqueous humor of glaucoma patients has been reported [57]. It seems that endothelin, the release of which has been shown to be stimulated by stretch and fluid flow rate [58], might be an important hormone regulating aqueous humor production and/or outflow.…”

Section: Contractility Measurementsmentioning

confidence: 99%

Regulation of Trabecular Meshwork Contractility

Stumpff

Wiederholt²

2000

Ophthalmologica

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Ample evidence supports the theory that trabecular meshwork possesses smooth-muscle-like properties. Trabecular meshwork cells express a large number of transporters, channels and receptors, many of which are known to regulate smooth-muscle contractility. It has been shown that trabecular meshwork can be induced to contract and relax in response to pharmacological agents. In the model of the bovine eye, confirmed in some cases by experiments on primates, agents that contract trabecular meshwork reduce outflow. On the cellular level, this is coupled with depolarization and a rise in intracellular calcium. Relaxation of trabecular meshwork, on the other hand, appears to be coupled to a stimulation of the maxi-K channel, inducing hyperpolarization and a closure of L-type calcium channels. No significant differences between cells from a human and a bovine source emerged, either in classical measurements of membrane voltage, in measurements of intracellular calcium or patch-clamp experiments. Thus, pharmacological agents that relax trabecular meshwork seem promising candidates for further research – the ultimate goal being an improvement of glaucoma therapy in humans.

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Section: Contractility Measurementsmentioning

confidence: 99%

Regulation of Trabecular Meshwork Contractility

Stumpff

Wiederholt²

2000

Ophthalmologica

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“…Increased levels of ET-1 are found in acute renal failure, hypertension, heart failure, ischemic heart disease, Prinzmetal angina, pulmonary hypertension, Raynaud's disease, subarachnoid hemorrhage, cerebral vasospasm, migraine and diabetes [5,9]. EG-1 is normally found in the eye, where it is produced by the non-pigmented ciliary epithelium and is released into the intraocular liquid [10]. Its receptors are expressed upon various structures, like iris, ciliary muscle, trabecular meshwork (TM), vasculature, retinal and optic nerve astrocytes, which determines the physiological role of ET-1 in the eye [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Plasma endothelin-1 and endothelin-A receptor concentrations in patients with primary open-angle glaucoma

Mihaylova

Petkova

Rankova-Yotova

et al. 2017

Biotechnology & Biotechnological Equipment

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Endothelin-1 (ET-1) is a potent vasoconstrictor and is considered to have a key role in the regulation of ocular perfusion and glaucoma pathogenesis. High ET-1 and ET A -receptor levels are reported in patients with primary open-angle glaucoma (POAG). We compared the mean plasma ET-1 and ET Areceptor concentration of controls and patients with early and advanced POAG stage, and assessed the correlation with the retinal nerve fibre layer (RNFL) thickness. The study included a total of 75 participants, aged 45-83 years: 25 (controls), 22 (early glaucoma) and 28 (advanced glaucoma). The plasma concentration of ET-1 and ET A -receptor was determined by enzyme-linked immunosorbent assay. The RNFL thickness was evaluated with spectral-domain optical coherence tomography. The mean ET-1 concentration was lower in the control group (4.88 § 1.75 pg/mL) than in the early and advanced POAG group (6.33 § 2.38 and 6.34 § 1.56 pg/mL). Statistically significant difference was found between the mean ET-1 concentrations in controls and glaucoma patients (p = 0.029 -early glaucoma, p = 0.018 -advanced glaucoma), and no significant difference was observed between the two POAG groups (p = 0.998). The mean ET A -receptor concentration was highest in the control group (1209.28 § 314.48 pg/mL) and the differences between the three groups were significant. Significant relationship was found only between ET-1 and RNFL. This study demonstrated the role of ET-1 in glaucoma pathogenesis based on the observed significant high ET-1 and ET A -receptor plasma levels in POAG patients. A new therapeutical approach needs to be considered in some patients.

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“…32,33 Et-1 is also found in the aqueous humor at concentrations several times higher than in plasma, presumably because it is secreted by the ciliary epithelium and not derived from plasma. 34 Endothelin binds primarily with 2G-protein coupled receptors, Endothelin A(ETA), located primarily in vascular smooth-muscle cell, and Endothelin B (ETB), located primarily in endothelial cells, neurons, and glia. The actions of the Endothelin are probably not limited to maintaining vascular tone and blood flow, but the action of ET-1 on ETA results in vasoconstriction and on ETB to nitric-oxide-mediated vasoconstriction.…”

Section: Endothelin and Its Receptorsmentioning

confidence: 99%