Effects of Nipradilol on Alpha-Adrenoceptor Function in Ocular Arteries

Okamura, Tomio; Fujioka, Hideyuki; Ayajiki, Kazuhide

doi:10.1159/000056195

Cited by 9 publications

(7 citation statements)

References 12 publications

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“…In patients with schizophrenia and visual disturbance, deterioration of the visual cortex and retinal thickness was discovered within three years of the patients beginning to take an antipsychotic agent [32]. Other scholars reported that cystoid macular edema induced by risperidone may be caused by, for example, the agent directly affecting the retinal vascular endothelium or vasorelaxation through alpha-adrenergic blockade [33]. Thus, whether clozapine affects the retina should be investigated, and the possible mechanism should be identified.…”

Section: Introductionmentioning

confidence: 99%

Clozapine Worsens Glucose Intolerance, Nonalcoholic Fatty Liver Disease, Kidney Damage, and Retinal Injury and Increases Renal Reactive Oxygen Species Production and Chromium Loss in Obese Mice

Chang

Liu

Yang

et al. 2021

IJMS

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Clozapine is widely employed in the treatment of schizophrenia. Compared with that of atypical first-generation antipsychotics, atypical second-generation antipsychotics such as clozapine have less severe side effects and may positively affect obesity and blood glucose level. However, no systematic study of clozapine’s adverse metabolic effects—such as changes in kidney and liver function, body weight, glucose and triglyceride levels, and retinopathy—was conducted. This research investigated how clozapine affects weight, the bodily distribution of chromium, liver damage, fatty liver scores, glucose homeostasis, renal impairment, and retinopathy in mice fed a high fat diet (HFD). We discovered that obese mice treated with clozapine gained more weight and had greater kidney, liver, and retroperitoneal and epididymal fat pad masses; higher daily food efficiency; higher serum or hepatic triglyceride, aspartate aminotransferase, alanine aminotransferase, blood urea nitrogen, and creatinine levels; and higher hepatic lipid regulation marker expression than did the HFD-fed control mice. Furthermore, the clozapine group mice exhibited insulin resistance, poorer insulin sensitivity, greater glucose intolerance, and less Akt phosphorylation; their GLUT4 expression was lower, they had renal damage, more reactive oxygen species, and IL-1 expression, and, finally, their levels of antioxidative enzymes (superoxide dismutase, glutathione peroxidase, and catalase) were lower. Moreover, clozapine reduced the thickness of retinal cell layers and increased iNOS and NF-κB expression; a net negative chromium balance occurred because more chromium was excreted through urine, and this influenced chromium mobilization, which did not help overcome the hyperglycemia. Our clozapine group had considerably higher fatty liver scores, which was supported by the findings of lowered adiponectin protein levels and increased FASN protein, PNPLA3 protein, FABP4 mRNA, and SREBP1 mRNA levels. We conclude that clozapine can worsen nonalcoholic fatty liver disease, diabetes, and kidney and retinal injury. Therefore, long-term administration of clozapine warrants higher attention.

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Section: Introductionmentioning

confidence: 99%

Clozapine Worsens Glucose Intolerance, Nonalcoholic Fatty Liver Disease, Kidney Damage, and Retinal Injury and Increases Renal Reactive Oxygen Species Production and Chromium Loss in Obese Mice

Chang

Liu

Yang

et al. 2021

IJMS

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“…It is reported that nipradilol increases ophthalmic circulation by direct activity on retinal vessels, and the activity is based on blocking the alpha 1 ‐receptor, which has been shown in cats, monkeys and humans 9,12,17 . In dogs it is reported that nipradilol extends vessels in vitro 19 . Thus, we expect that nipradilol increases ocular circulation in dogs.…”

Section: Discussionmentioning

confidence: 77%

“…Recently, ophthalmic circulation has been considered in the treatment of glaucoma 17–19 . It is reported that nipradilol increases ophthalmic circulation by direct activity on retinal vessels, and the activity is based on blocking the alpha 1 ‐receptor, which has been shown in cats, monkeys and humans 9,12,17 .…”

Section: Discussionmentioning

confidence: 99%

Effects of topical nipradilol and timolol maleate on intraocular pressure, facility of outflow, arterial blood pressure and pulse rate in dogs

Maehara

Ono

Ito

et al. 2004

Veterinary Ophthalmology

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Nipradilol is an alpha(1), beta-blocker with milder side effects than other beta-blockers used in humans. In this study the effects of nipradilol were compared with those of timolol maleate in dogs. Twelve clinically normal dogs (nine mongrels, two beagles, and one Akita) were used. We applied 0.25% nipradilol or 0.5% timolol maleate drops for a period of 28 days. Intraocular pressure (IOP) was measured before and after administration on the 2nd, 4th, 7th, 14th, 21st and 28th day. Blood pressure, pulse rate and coefficient of aqueous outflow (C-value) were also measured before and after administration on the 7th, 14th, 21st and 28th day. Both nipradilol and timolol maleate significantly lowered IOP from the 2nd day to the end of the study period. Nipradilol lowered IOP to an equivalent degree to timolol maleate. There was no significant change in blood pressure and pulse rate throughout the study period with administration of nipradilol. C-value showed a significant rise from the 14th day with administration of nipradilol, while it did not show any significant change during the study period with administration of timolol maleate. The reduction of IOP by nipradilol was similar to that by an existing beta-adrenergic antagonist, timolol maleate, but nipradilol was associated with fewer systemic side effects in dogs. Nipradilol appears to be a useful drug for treatment of glaucoma in dogs.

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“…These include a high affinity for serotonin receptors, a1-adrenergic and a2-adrenergic receptor blockade, and dopaminergic receptor blockade [5]. Research suggests that mechanisms such as vasorelaxation via alpha adrenergic blockade or direct effects on the retinal vascular endothelium may be responsible for risperidone-induced CME [6].…”

Section: Discussionmentioning

confidence: 99%

Risperidone-related bilateral cystoid macular edema: a case report

2019

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BackgroundA report of the second known case of bilateral cystoid macular edema in a patient taking risperidone.Case presentationWe report a case of a 69-year-old African American woman using risperidone who presented with worsening visual acuity and was found to have bilateral cystoid macular edema. Upon decreasing the dosage of risperidone, the cystoid macular edema resolved and visual acuity markedly improved. Fluorescein angiography and optical coherence tomography were used to document the severity of cystoid macular edema and subsequent resolution after decreased dosage of risperidone.ConclusionThe documentation of a patient who developed cystoid macular edema associated with risperidone usage indicates that it may be beneficial to monitor patients taking risperidone for the development of maculopathy.

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Effects of Nipradilol on Alpha-Adrenoceptor Function in Ocular Arteries

Cited by 9 publications

References 12 publications

Clozapine Worsens Glucose Intolerance, Nonalcoholic Fatty Liver Disease, Kidney Damage, and Retinal Injury and Increases Renal Reactive Oxygen Species Production and Chromium Loss in Obese Mice

Clozapine Worsens Glucose Intolerance, Nonalcoholic Fatty Liver Disease, Kidney Damage, and Retinal Injury and Increases Renal Reactive Oxygen Species Production and Chromium Loss in Obese Mice

Effects of topical nipradilol and timolol maleate on intraocular pressure, facility of outflow, arterial blood pressure and pulse rate in dogs

Risperidone-related bilateral cystoid macular edema: a case report

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