Histamine Induced Contraction of Human Ciliary Muscle Cells

Markwardt, Kerry L.; Magnino, Peggy E.; Iok-Houpang,

doi:10.1006/exer.1996.0255

Cited by 6 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Firstgeneration H1 antagonists have poor selectivity and demonstrate anti-muscarinic, anti-a-adrenergic, and anti-serotonin effects. 7 Both histamine H1 receptors and cholinergic muscarinic receptors are found in the ciliary body and mediate the contraction and relaxation of the ciliary body-zonule-lens complex, 8 which may alter the position of the IOL and result in acute myopia. Cases of acute myopia secondary to topiramate are similarly well-described in the literature.…”

Section: Discussionmentioning

confidence: 99%

Late-onset capsular bag distension syndrome following antihistamine administration

Haberman

Rusu

Kahn

2014

Journal of Cataract and Refractive Surgery Online Case Reports

View full text Add to dashboard Cite

A 51-year-old woman presented with acute myopic shift 3 years after uneventful cataract extraction in both eyes; recent medical history was remarkable for administration of intravenous meclizine 2 weeks prior to presentation. Examination of each eye revealed anterior chamber crowding and a posterior chamber intraocular lens (IOL) with distension of the capsular bag; clear fluid with a green hue was present between the IOL and the posterior capsule. We postulate a mechanism for the development of late-onset capsular bag distension syndrome. To our knowledge, no medication-induced incidences have been reported in the literature. Financial Disclosure: No author has a financial or proprietary interest in any material or method mentioned. JCRS Online Case Reports 2014; 2:58-60 Q 2014 ASCRS and ESCRSCapsular block is a rare complication of cataract surgery with posterior chamber intraocular lens (PC IOL) implantation following a continuous curvilinear capsulorhexis (CCC). Capsular block is traditionally classified by its time of onset: intraoperative, early postoperative, or late postoperative. 1 The mechanism of late postoperative capsular block involves the accumulation of particulate matter posterior to the IOL, which draws aqueous humor posterior to the IOL via osmosis. 2 We describe a unique case of late-onset capsular block secondary to a systemic antihistamine and hypothesize a mechanism for the development of capsular block. CASE REPORTA 51-year-old Asian woman presented complaining of acutely decreased vision at distance and improved vision at near. The ocular history was significant for uneventful cataract extraction with bilateral implantation of a 1-piece acrylic PC IOL 3 years previously. On examination 3 months before presentation, the uncorrected distance visual acuity was 20/20 in both eyes; dilated fundoscopy was unremarkable, with monofocal acrylic 1-piece IOLs positioned in the capsular bag; and there was no anterior capsule fibrosis or fluid accumulation behind the IOLs. The recent medical history was remarkable for vertigo, for which the patient had been admitted to the hospital and administered intravenous meclizine 2 weeks previously.On examination, the corrected distance visual acuity (CDVA) was 20/20 with a manifest refraction of À1.50 À1.00 Â 165 in the right eye and 20/20 with a manifest refraction of À1.50 À0.25 Â 15 in the left eye. Slitlamp examination was remarkable for anterior chamber crowding in both eyes. Gonioscopy revealed a 360-degree grade III ciliary body in both eyes with mild plateau iris configuration. Intraocular pressure was 15 mm Hg in the right eye and 17 mm Hg in the left eye. Dilated examination was remarkable for a PC IOL in each eye, with appreciable distension of the capsular bags and clear fluid with a green hue posterior to both IOLs (Figure 1).Humphrey visual field testing was within normal limits in both eyes, as was optical coherence tomography (OCT) of the macula. Optical coherence tomography of the angle showed slight anterior displacement of the iris in both e...

show abstract

Section: Discussionmentioning

confidence: 99%

Late-onset capsular bag distension syndrome following antihistamine administration

Haberman

Rusu

Kahn

2014

Journal of Cataract and Refractive Surgery Online Case Reports

View full text Add to dashboard Cite

show abstract

“…Histamine could interact with the H 1 receptor, a G-protein receptor (Gq), on the cell surface and activates phospholipase C and the phosphatidylinositol signal pathway, thus increasing intracellular calcium inducing cell contraction (Figure 6). Histamine, via H 1 R, stimulates the production of inositol phosphate and mobilization of intracellular Ca 2+ in cultured human ciliary muscle cells, reducing IOP [9,16].…”

Section: Discussionmentioning

confidence: 99%

“…The histamine neurons are located exclusively in the posterior hypothalamus from which they project to most areas of the central nervous system and also to the retina via retinopetal axons [8]. Histamine is responsible for ciliary muscle contraction in human eyes and, therefore, for IOP reduction [9]. Taken together, this evidence supports a potential role of histamine in the regulation of IOP.…”

Section: Introductionmentioning

confidence: 93%

Role of Histamine H3 Receptor Antagonists on Intraocular Pressure Reduction in Rabbit Models of Transient Ocular Hypertension and Glaucoma

Lanzi

Lucarini

Durante

et al. 2019

IJMS

View full text Add to dashboard Cite

Intraocular pressure (IOP) has a tendency to fluctuate throughout the day, reaching its peak in the early morning in healthy subjects or glaucoma patients. Likewise, histamine tone also fluctuates over time, being lower at nighttime. Numerous studies have demonstrated a correlation between short-term IOP fluctuation and glaucoma progression; however, it has not yet been determined whether histamine plays a role in IOP fluctuations. The aim of this research was to establish the distribution of the histamine receptor proteins and respective mRNAs in the eye by western blot, immunohistochemistry and RT-PCR in New Zealand rabbits. Furthermore, we used a transient ocular hypertension (OHT) model induced by injection of 50 µL of 5% hypertonic saline into the vitreous and a stable OHT model (100 µL 0.1% carbomer in the anterior chamber) to address the potential IOP-lowering ability of H3 receptor (H3R) antagonists (ciproxifan, DL76 and GSK189254). IOPs were performed with a Tono-Pen at baseline and 60, 120 and 240 min post treatment after transient OHT induction and, every day for 12 days in the stable OHT model. All histamine receptor subtypes were localized in the rabbit retina and ciliary body/trabecular meshwork. All the treatments lowered IOP in a dose-dependent fashion between 0.3% and 1%. More specifically, the effects were maximal with ciproxifan at 60 min post-dose (IOP60 change = −18.84 ± 4.85 mmHg, at 1%), remained stable until 120 min (IOP120 change = −16.38 ± 3.8 mmHg, at 1%) and decayed thereafter to reach baseline values at 240 min. These effects were highly specific and dependent on histamine release as pre-treatment with imetit (H3R agonist, 1%) or pyrilamine (H1R antagonist, 1%) largely blocked ciproxifan-mediated effects. Color Doppler ultrasound examination was performed to evaluate changes in ophtalmic artery resistivity index (RI) before and after repeated dosing with DL 76, GSK189254, ciproxifan and timolol. Chronic treatments with H3R antagonists and timolol improved the vascular performance of ophthalmic arteries and reduced retinal ganglion cell death. Oxidative stress was also reduced and measured 8-Hydroxy-2′-deoxyguanosine (8OHdG) expression, and by dihidroethydium (DHE) staining. These results demonstrated that the histamine system participates in IOP regulation and that H3R antagonists could represent a future promising therapy for glaucoma. Further studies should be focused on the long-term IOP circadian fluctuations.

show abstract

“…So far, many components have been studied regarding their ability to induce contraction of ciliary muscle samples. These include muscarinic agonists, mainly M 3 subtype (acting through phospholipase C activity and intracellular calcium accumulation, in a G q/11 -coupled pathway) (Yasui et al 2008); CB 1 -agonist, anandamide, which induces contraction (dependent on phospholipase C and βγ subunit of G i /G o proteins), alone or synergistically with carbachol (Lograno andRomano 2004, Romano andLograno 2013); endothelin-1, through ET A receptor activation (though, in low-doses, it elicits relaxation, via ET B receptors) (Kamikawatoko et al 1995); serotonin, through 5-HT 2 and 5-HT 3 receptors (Lograno and Romano 2003) and histamine, via H 1 receptors, which activates phospholipase C and increases intracellular calcium (Markwardt et al 1997). Moreover, ciliary muscle contraction can be provoked through membranebound PKC stimulation (using phorbol 12-myristate 13-acetate) (Thieme et al 1999) or inhibition of PKC, using staurosporin or H7, causing potentiation of carbachol contraction (Lograno et al 1991, Daniele et al 1997; PDEI (N-ethylmaleimide and iodoacetic acid) (Yoshino and Suzuki 1992); epidermal growth factorurogastrone (EGF) (Wiederholt et al 1998); substance P (Lograno and Daniele 1988) and 4-aminopyridine, a potassium channel blocking drug, which appears to potentiate the evoked ciliary muscle contractions without changing resting tension (Zacharias and Guerrero 1985).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Iris Sphincter and Ciliary Muscles by Urocortin 2

Tavares-Silva

Santos-Ferreira²,

Cardoso³

et al. 2018

Physiol Res

View full text Add to dashboard Cite

Urocortin 2 (UCN2) is a peptide related to corticotropin-releasing factor, capable of activating CRF-R2. Among its multisystemic effects, it has actions in all 3 muscle subtypes. This study's aim was to determine its potential role in two of the intrinsic eye muscle kinetics. Strips of iris sphincter (rabbit) and ciliary (bovine) muscles were dissected and mounted in isometric forcetransducer systems filled with aerated-solutions. Contraction was elicited using carbachol (10 -6 M for iris sphincter, 10 -5 M for ciliary muscle), prior adding to all testing substances. UCN2 induced relaxation in iris sphincter muscle, being the effect maximal at 10 -7 M concentrations (-12.2 % variation vs. control). This effect was abolished with incubation of indomethacin, antisauvagine-30, chelerytrine and SQ22536, but preserved with L-nitro-L-arginine. In carbachol pre-stimulated ciliary muscle, UCN2 (10 -5 M) enhanced contraction (maximal effect of 18.2 % increase vs. control). UCN2 is a new modulator of iris sphincter relaxation, dependent of CRF-R2 activation, synthesis of prostaglandins (COX pathway) and both adenylate cyclase and PKC signaling pathways, but independent of nitric oxide production. Regarding ciliary muscle, UCN2 enhances carbachol-induced contraction, in higher doses.

show abstract

Histamine Induced Contraction of Human Ciliary Muscle Cells

Cited by 6 publications

References 0 publications

Late-onset capsular bag distension syndrome following antihistamine administration

Late-onset capsular bag distension syndrome following antihistamine administration

Role of Histamine H3 Receptor Antagonists on Intraocular Pressure Reduction in Rabbit Models of Transient Ocular Hypertension and Glaucoma

Modulation of Iris Sphincter and Ciliary Muscles by Urocortin 2

Contact Info

Product

Resources

About