ArticleInvestigative ophthalmology & visual science2011
Vulnerability of the retinal microvasculature to hypoxia: role of polyamine-regulated K(ATP) channels.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
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- Optical cohorence tomography angiography findings in carotid artery stenosis.International ophthalmology · 2022Article
- Optical Coherence Tomography Angiography Evaluation of Retinal Microvasculature Before and After Carotid Angioplasty and Stenting.Scientific reports · 2019Article
- Retinal ischemia induces α-SMA-mediated capillary pericyte contraction coincident with perivascular glycogen depletion.Acta neuropathologica communications · 2019Article
- Purinergic Vasotoxicity: Role of the Pore/Oxidant/KVision (Basel, Switzerland) · 2018Article
- Role of ion channels in the functional response of conjunctival goblet cells to dry eye.American journal of physiology. Cell physiology · 2018Article
- Angiogenic neovessels promote tissue hypoxia.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Bioelectric impact of pathological angiogenesis on vascular function.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- 8-iso-prostaglandin-F2α: a possible trigger or accelerator of diabetic retinopathy.International journal of ophthalmology · 2016Article
- Descending vasa recta endothelial cells and pericytes form mural syncytia.American journal of physiology. Renal physiology · 2014Article
- Retinovascular physiology and pathophysiology: new experimental approach/new insights.Progress in retinal and eye research · 2012Review
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2 authors.
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Abstract
purposeIt is uncertain why retinal capillaries are particularly vulnerable to hypoxia. In this study, it was hypothesized that their specialized physiology, which includes being the predominant microvascular location of functional adenosine triphosphate-sensitive potassium (K(ATP)) channels, boosts their susceptibility to hypoxia-induced cell death.
methodsCell viability, ionic currents, intracellular calcium, and pericyte contractility in microvascular complexes freshly isolated from the rat retina were assessed using trypan blue dye exclusion, perforated-patch recordings, fura-2 fluorescence, and time-lapse videos. Chemical hypoxia was induced by antimycin, an oxidative phosphorylation inhibitor.
resultsIn freshly isolated retinal microvascular complexes, chemical hypoxia caused more cell death in capillaries than in arterioles. Indicative of the role of polyamine-dependent K(ATP) channels, antimycin-induced capillary cell death was markedly decreased in microvessels treated with the polyamine synthesis inhibitor, difluoromethylornithine, or the K(ATP) channel inhibitor, glibenclamide. These inhibitors also diminished the antimycin-induced hyperpolarization, as well as the antimycin-induced intracellular calcium increase, which was significantly dependent on extracellular calcium and was diminished by the inhibitor of calcium-induced calcium release (CICR), dantrolene. Consistent with the importance of the CICR-dependent increase in capillary cell calcium, dantrolene significantly decreased hypoxia-induced capillary cell death. We also found that activation of the polyamine/K(ATP) channel/Ca(2+) influx/CICR pathway not only boosted the vulnerability of retinal capillaries to hypoxia, but also caused the contraction of capillary pericytes, whose vasoconstrictive effect may exacerbate hypoxia.
conclusionsThe vulnerability of retinal capillaries to hypoxia is boosted by a mechanism involving the polyamine/K(ATP) channel/Ca(2+) influx/CICR pathway. Discovery of this pathway should provide new targets for pharmacological interventions to minimize hypoxia-induced damage in retinal capillaries.
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