ArticleInvestigative ophthalmology & visual science2010
Diabetes-induced inhibition of voltage-dependent calcium channels in the retinal microvasculature: role of spermine.
Article in Investigative ophthalmology & visual science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Distinct potassium channel types in brain capillary pericytes.Biophysical journal · 2024Article
- Orai, RyR, and IPCommunications biology · 2023Article
- Pericyte dysfunction and loss of interpericyte tunneling nanotubes promote neurovascular deficits in glaucoma.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Cerebrovascular and neurological perspectives on adrenoceptor and calcium channel modulating pharmacotherapies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Review
- Acrolein: A Potential Mediator of Oxidative Damage in Diabetic Retinopathy.Biomolecules · 2020Review
- Type 2 diabetes and HbADiabetologia · 2020Article
- The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020Review
- Electrotonic transmission in the retinal vasculature: inhibitory role of the diabetes/VEGF/aPKC pathway.Physiological reports · 2019Article
- Purinergic Vasotoxicity: Role of the Pore/Oxidant/KVision (Basel, Switzerland) · 2018Article
- Role of capillary pericytes in the integration of spontaneous CaThe Journal of physiology · 2018Article
- Layer-Specific Manganese-Enhanced MRI of the Diabetic Rat Retina in Light and Dark Adaptation at 11.7 Tesla.Investigative ophthalmology & visual science · 2015Article
- High-Fat Diet-Induced Retinal Dysfunction.Investigative ophthalmology & visual science · 2015Article
- Role of ACE and PAI-1 Polymorphisms in the Development and Progression of Diabetic Retinopathy.PloS one · 2015Article
- Angiotensin II-related hypertension and eye diseases.World journal of cardiology · 2014Review
- Diabetic retinopathy: loss of neuroretinal adaptation to the diabetic metabolic environment.Annals of the New York Academy of Sciences · 2014Review
- Arginase in retinopathy.Progress in retinal and eye research · 2013Review
- The electrotonic architecture of the retinal microvasculature: diabetes-induced alteration.Neurochemistry international · 2012Article
- Cellular and physiological mechanisms underlying blood flow regulation in the retina and choroid in health and disease.Progress in retinal and eye research · 2012Review
- Vulnerability of the retinal microvasculature to oxidative stress: ion channel-dependent mechanisms.American journal of physiology. Cell physiology · 2012Article
- Retinovascular physiology and pathophysiology: new experimental approach/new insights.Progress in retinal and eye research · 2012Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
purposeAlthough decentralized control of blood flow is particularly important in the retina, knowledge of the functional organization of the retinal microvasculature is limited. Here, the authors characterized the distribution and regulation of L-type voltage-dependent calcium channels (VDCCs) within the most decentralized operational complex of the retinal vasculature--the feeder vessel/capillary unit--which consists of a capillary network plus the vessel linking it with a myocyte-encircled arteriole.
methodsPerforated-patch recordings, calcium-imaging, and time-lapse photography were used to assess VDCC-dependent changes in ionic currents, intracellular calcium, abluminal cell contractility, and lumen diameter, in microvascular complexes freshly isolated from the rat retina.
resultsTopographical heterogeneity was found in the distribution of functional VDCCs; VDCC activity was markedly greater in feeder vessels than in capillaries. Experiments showed that this topographical distribution occurs, in large part, because of the inhibition of capillary VDCCs by a mechanism dependent on the endogenous polyamine spermine. An operational consequence of functional VDCCs predominantly located in the feeder vessels is that voltage-driven vasomotor responses are generated chiefly in this portion of the feeder vessel/capillary unit. However, early in the course of diabetes, this ability to generate voltage-driven vasomotor responses becomes profoundly impaired because of the inhibition of feeder vessel VDCCs by a spermine-dependent mechanism.
conclusionsThe regulation of VDCCs by endogenous spermine not only plays a critical role in establishing the physiological organization of the feeder vessel/capillary unit, but also may contribute to dysfunction of this decentralized operational unit in the diabetic retina.
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