scholarly journals Involvement of trabecular meshwork phagocytic suppression by sympathetic norepinephrine in nocturnal intraocular pressure rise

2021 ◽  
Author(s):  
Keisuke Ikegami ◽  
Satoru Masubuchi
Keyword(s):  
Circadian Rhythm ◽  
Intraocular Pressure ◽  
Trabecular Meshwork ◽  
Adrenergic Receptor ◽  
Ciliary Body ◽  
Pressure Rise ◽  
Inhibitory Effect ◽  
Pharmacological Prevention ◽  
Signal Activation

Abstract Intraocular pressure (IOP) is important in glaucoma development and depends on aqueous humor (AH) dynamics, involving inflow from the ciliary body and outflow through the trabecular meshwork (TM). IOP has a circadian rhythm entrained by sympathetic noradrenaline (NE) or adrenal glucocorticoids (GCs). Here, we investigated the involvement of GC and NE in AH outflow. Pharmacological prevention of inflow/outflow in mice indicated an AH outflow increase during day. Although TM phagocytosis can determine AH drainage, only NE showed a non-self-sustained inhibitory effect in phagocytosis of immortalized human TM cells. Pharmacological approach and RNA interference identified β1-adrenergic receptor (AR)-mediated cAMP-EPAC-SHIP1 signal activation by ablation of phosphatidylinositol triphosphate regulating phagocytic cup formation. Furthermore, pharmacological instillation in mice revealed the role of β1-AR-EPAC-SHIP1 pathway in nocturnal IOP rise. These suggest that IOP rhythm is partially regulated by this pathway. This first demonstration of TM phagocytosis suppression by NE could be useful in glaucoma management.

scholarly journals Role of beta-adrenergic receptor subtypes in pig uterus contractility with inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Barbara Jana ◽  
Jarosław Całka
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Domestic Animals ◽  
Inhibitory Effect ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptor ◽  
Pharmacological Modulation ◽  
Uterine Inflammation ◽  
Myometrial Contractility

AbstractUterine inflammation is a very common and serious condition in domestic animals. To development and progression of this pathology often lead disturbances in myometrial contractility. Participation of β1-, β2- and β3-adrenergic receptors (ARs) in noradrenaline (NA)-influenced contractility of the pig inflamed uterus was studied. The gilts of SAL- and E.coli-treated groups were administered saline or E.coli suspension into the uterine horns, respectively. Laparotomy was only done in the CON group. Compared to the period before NA administration, this neurotransmitter reduced the tension, amplitude and frequency in uterine strips of the CON and SAL groups. In the E.coli group, NA decreased the amplitude and frequency, and these parameters were lower than in other groups. In the CON, SAL and E.coli groups, β1- and β3-ARs antagonists in more cases did not significantly change and partly eliminated NA inhibitory effect on amplitude and frequency, as compared to NA action alone. In turn, β2-ARs antagonist completely abolished NA relaxatory effect on these parameters in three groups. Summarizing, NA decreases the contractile amplitude and frequency of pig inflamed uterus via all β-ARs subtypes, however, β2-ARs have the greatest importance. Given this, pharmacological modulation of particular β-ARs subtypes can be used to increase inflamed uterus contractility.

scholarly journals Transcriptome analysis reveals autophagy as regulator of TGFβ/Smad-induced fibrogenesis in trabecular meshwork cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
April Nettesheim ◽  
Myoung Sup Shim ◽  
Josh Hirt ◽  
Paloma B. Liton
Keyword(s):  
Intraocular Pressure ◽  
Transcriptome Analysis ◽  
Trabecular Meshwork ◽  
Ocular Tissue ◽  
Primary Cells ◽  
Tgfβ Signaling ◽  
Transcript Levels ◽  
Trabecular Meshwork Cells ◽  
Network Analyses

Abstract The trabecular meshwork (TM) is a specialized ocular tissue, which is responsible, together with the Schlemm’s canal (SC), for maintaining appropriate levels of intraocular pressure. Dysfunction of these tissues leads to ocular hypertension and increases the risk for developing glaucoma. Previous work by our laboratory revealed dysregulated autophagy in aging and in glaucomatous TM cells. In order to gain more insight in the role of autophagy in the TM pathophysiology, we have conducted transcriptome and functional network analyses of TM primary cells with silenced expression of the autophagy genes Atg5 and Atg7. Atg5/7-deficient TM cells showed changes in transcript levels of several fibrotic genes, including TGFβ2, BAMBI, and SMA. Furthermore, genetic and pharmacological inhibition of autophagy was associated with a parallel reduction in TGFβ-induced fibrosis, caused by a BAMBI-mediated reduced activation of Smad2/3 signaling in autophagy-deficient cells. At the same time, TGFβ treatment led to Smad2/3-dependent dysregulation of autophagy in TM cells, characterized by increased LC3-II levels and autophagic vacuoles content. Together, our results indicate a cross-talk between autophagy and TGFβ signaling in TM cells.

The Role of the Vitreous in the Intraocular Pressure Rise After Neodymium-YAG Laser Capsulotomy

1985 ◽  
Vol 103 (10) ◽  
pp. 1538-1542 ◽  
Author(s):  
H. D. Schubert ◽  
W. J. Morris ◽  
S. L. Trokel ◽  
E. A. Balazs
Keyword(s):  
Intraocular Pressure ◽  
Pressure Rise ◽  
Yag Laser ◽  
Neodymium Yag Laser

scholarly journals The Effects of Prostaglandin Analogs on Intraocular Pressure in Human Eye for Open Angle Glaucoma

2020 ◽  
Vol 10 (2) ◽  
pp. 176-180
Author(s):  
Shabab Akbar ◽  
Sapna Ratan Shah
Keyword(s):  
Fluid Flow ◽  
Intraocular Pressure ◽  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Ciliary Body ◽  
Open Angle Glaucoma ◽  
Posterior Chamber ◽  
Open Angle ◽  
Permeable Channel ◽  
Aqueous Outflow

The effects of Prostaglandin Analogs on intraocular pressure and increased aqueous outflow via trabecular meshwork into the schlemm’s canal has been studied in this present research paper. Aqueous humor is an outflow, which flows at the back of the iris in the posterior chamber all the way through the pupil aperture, out into the anterior chamber, and drain from the eye via drainage slope. The eye keeps on making aqueous humor in the ciliary body and it passes through the trabecular meshwork into the scheme of the canal, the key drainage from the eye and it finally goes to the “collector channels” and due to the less amount of aqueous humor fluid flow from the drainage angle, the pressure in the eye starts to increase. For this study, the canal of Schlemm is assumed as a permeable channel. And it is connected by trabecular meshwork. The inner layer of the canal's wall has been assumed as permeable. And the aqueous humor drains into the canal through this porous tissue wall. The objective of this paper is to discuss the effect of prostaglandin analogs on intraocular pressure as the Prostaglandin Analogs work by increasing the outflow of aqueous from the eye.

scholarly journals Novel Insight of Histamine and Its Receptor Ligands in Glaucoma and Retina Neuroprotection

Biomolecules ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1186
Author(s):  
Silvia Sgambellone ◽  
Laura Lucarini ◽  
Cecilia Lanzi ◽  
Emanuela Masini
Keyword(s):  
Risk Factors ◽  
Circadian Rhythm ◽  
Intraocular Pressure ◽  
Animal Models ◽  
Receptor Ligands ◽  
Short Term ◽  
Future Treatment ◽  
Progressive Degeneration ◽  
Histamine H3

Glaucoma is a multifactorial neuropathy characterized by increased intraocular pressure (IOP), and it is the second leading cause of blindness worldwide after cataracts. Glaucoma combines a group of optic neuropathies characterized by the progressive degeneration of retinal ganglionic cells (RGCs). Increased IOP and short-term IOP fluctuation are two of the most critical risk factors in glaucoma progression. Histamine is a well-characterized neuromodulator that follows a circadian rhythm, regulates IOP and modulates retinal circuits and vision. This review summarizes findings from animal models on the role of histamine and its receptors in the eye, focusing on the effects of histamine H3 receptor antagonists for the future treatment of glaucomatous patients.

Glaucoma Problems Associated with Aniridia

2010 ◽  
Author(s):  
Peter A. Netland
Keyword(s):  
Intraocular Pressure ◽  
Anterior Chamber ◽  
Trabecular Meshwork ◽  
Ciliary Body ◽  
Vision Loss ◽  
Visual Field Loss ◽  
Anterior Chamber Angle ◽  
Foveal Hypoplasia ◽  
Closed Angle ◽  
Chamber Angle

Glaucoma is a potentially vision-threatening problem that is commonly encountered in aniridia patients. This condition may develop at birth, or shortly thereafter. More commonly, however, glaucoma is acquired later in childhood or even young adulthood. If unrecognized and untreated, glaucoma can result in blindness. For this reason, it is important to be vigilant in watching for this condition in children affected with aniridia. Vision lost due to glaucomatous damage cannot be regained at a later time. In addition to glaucoma, children with aniridia may demonstrate other problems with their vision. They may have refractive errors, corneal or retinal problems, or abnormalities of eye movement. Foveal hypoplasia (lack of development of the retina) may limit vision in some children. In aniridia patients, cataract (opacification or cloudiness of the lens) is seen with approximately the same prevalence as glaucoma. Cataract, however, differs from glaucoma in that the vision loss due to cataract is reversible. Glaucoma is suspected in aniridia patients when there is an increased intraocular pressure. Glaucoma can be definitely diagnosed when changes of the optic nerve occur due to this elevated intraocular pressure. At the later stages of the disease, visual field loss occurs. In the normal eye, the fluid (aqueous humor) in the front of the eye (the anterior chamber) is produced by the ciliary body, which is located behind the iris (see Figure 5.1). The fluid produced from the ciliary body flows forward into the anterior chamber, where it drains from the anterior chamber angle through tissue called the trabecular meshwork. When there is an abnormal situation, the fluid exits the eye poorly or not at all, and the intraocular pressure may be increased. The fluid may be blocked from exiting the eye by a closed angle, or may flow poorly out of the eye even though the angle is open (see Figure 5.2). The angle may be closed in aniridic patients when the stump of residual iris covers the trabecular meshwork in the anterior chamber angle.

The role of the hypothalamic β-adrenergic system in controlling the LH rise in short-term castrated rats

1987 ◽  
Vol 114 (2) ◽  
pp. 167-172 ◽  
Author(s):  
M. H. Al-Hamood ◽  
D. P. Gilmore ◽  
C. A. Wilson ◽  
P. Tuohy-Jones ◽  
S. Drummond ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Concomitant Administration ◽  
Inhibitory Effect ◽  
Adrenergic System ◽  
Receptor Subtypes ◽  
Short Term ◽  
Pharmacological Agents ◽  
Inhibitory Component ◽  
Lh Release

ABSTRACT Intraventricular infusions of adrenaline and various pharmacological agents acting on β-adrenergic receptor subtypes were carried out in rats orchidectomized 16 h previously. Infusions (10 μl) of solutions containing the drugs were administered under anaesthesia induced with alphaxalone and alphadolone. Levels of LH were measured in plasma collected immediately before and at predetermined intervals after the infusion. The acute rise in LH levels after castration was increased still further by isoprenaline (a mixed β1- and β2-agonist), fenoterol (a β2-agonist) and atenolol (a β1-antagonist). In contrast, prenalterol (a β1-agonist) and (2RS,3RS)-3-isopropylamino-1-(7-methylindan-4-yloxy)butan-2-ol (ICI 118 551) (a selective β2-antagonist) were inhibitory to LH release. Adrenaline itself, salbutamol (another selective β2-agonist), propranolol (a mixed β-antagonist) and metoprolol (a β1-antagonist) did not significantly alter plasma LH concentrations at the doses administered. The stimulatory effect of isoprenaline on LH release was partially reduced when given together with ICI 118 551, but was not affected when administered simultaneously with atenolol. The inhibitory effect of ICI 118 551 was, however, prevented by concomitant administration with fenoterol, as was that of prenalterol when infused with atenolol. The results suggest that the hypothalamic mediation of the short-term changes in LH release in response to castration is exerted, at least in part, through the activation of a β2-stimulatory component and the suppression of a β1-inhibitory component. J. Endocr. (1987) 114, 167–172

Effect of Dipyridamole on Spontaneous Platelet Aggregation in Whole Blood Decreases with the Time After Venepuncture: Evidence for the Role of ADP

1987 ◽  
Vol 58 (02) ◽  
pp. 744-748 ◽  
Author(s):  
A R Saniabadi ◽  
G D O Lowe ◽  
J C Barbenel ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Correlation Coefficient ◽  
Whole Blood ◽  
Blood Platelet ◽  
Inhibitory Effect ◽  
Time Interval ◽  
Adp Receptor ◽  
Spontaneous Platelet Aggregation

SummarySpontaneous platelet aggregation (SPA) was studied in human whole blood at 3, 5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter, SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of citrated blood at 37° C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10 μM at each time interval; (b) 0.5-100 μM at 3 and 30 minutes and (c) 15 μM in combination with 100 μM adenosine, 8 μM 2-chloroadenosine (2ClAd, an ADP receptor blocker) and 50 μM aspirin. There was a rapid decrease in the inhibitory effect of Dipy with the time after venepuncture; the correlation coefficient was -0.533. At all the concentrations studied, Dipy was more effective at 3 minutes than at 30 minutes after venepuncture. A combination of Dipy with adenosine, 2ClAd or aspirin was a more effective inhibitor of SPA than either drug alone. However, when 15 μM Dipy and 10 μM Ad were added together, the inhibitory effect of Dipy was not increased significantly, suggesting that Dipy inhibits platelet aggregation independent of Ad. The increase in SPA with the time after venepuncture was abolished when blood was taken directly into the anticoagulant containing 5 μM 2ClAd. It is suggested that ADP released from the red blood cells is responsible for the increased platelet aggregability with the time after venepuncture and makes a serious contribution to the artifacts of in vitro platelet function studies.

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