Suppression of Sodium-Dependent Glucose Uptake by Captopril Improves High-Glucose-Induced Morphological and Functional Changes of Cultured Bovine Retinal Pericytes

Wakisaka, Masanori; Yoshinari, Mototaka; Nakamura, Shin; Asano, Tomonari; Sonoki, Kazuo; Shi, Ai-Hong; Iwase, Masanori; Takata, Yutaka; Fujishima, Masatoshi

doi:10.1006/mvre.1999.2178

Cited by 21 publications

(15 citation statements)

References 26 publications

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“…Consequently, also based on in vitro evidence that angiotensin II increases glucose uptake by retinal pericytes [100], induces release of VEGF by retinal endothelial cells [101], and that blockade of the renin-angiotensin system could prevent new vessel growth in a transgenic animal model of retinopathy of prematurity [102], an angiotensin-receptor blocker is undergoing a clinical trial appropriately targeted and powered to test its possible role in the primary and secondary prevention of DR.…”

Section: Treatment Of Hypertension and Diabetic Retinopathymentioning

confidence: 99%

Diabetic retinopathy

2002

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Abstract. Easy observation of the fundus oculi makes retinopathy the most frequently reported chronic complication of diabetes and, consequently, the one we know best in terms of epidemiology and natural history. Achieving near-normal levels of blood glucose and blood pressure provides empirical though powerful tools for clinicians to delay the onset and progression of diabetic retinopathy. Even when these measures have failed and retinopathy becomes sight-threatening, laser photocoagulation has proven remarkably effective. Nonetheless, retinopathy remains a leading cause of blindness and there is little evidence that diabetes-related visual loss is decreasing in industrialized countries. This may result from the mixed blessing of prolonged survival of patients who had become diabetic when metabolic control was pursued less fastidiously than today. Screening for sight-threatening retinopathy is the most cost-effective medical procedure known and should help optimise the use of diagnostic and therapeutic resources, but its widest deployment still meets with inertia and lack of interest within most health care systems. Improving clinical skills and technology, however, allow us to take a more optimistic look at the future, as pathogenesis-targeted forms of treatment are being developed and tested through appropriately powered clinical trials. [Diabetologia (2002[Diabetologia ( ) 45:1617[Diabetologia ( -1634

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Section: Treatment Of Hypertension and Diabetic Retinopathymentioning

confidence: 99%

Diabetic retinopathy

2002

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“…Moreover, ANG- ( 1 - 7 ) is able to modulate insulin signaling pathway through the activation of IRS-1, JAK2, and Akt kinase in the main target tissues for insulin ( 54 , 55 ). Also, ACEIs can probably regulate glucose concentration by affecting the production and the activity of glucose transporters ( 42 , 56 , 57 ). To summarize, ACEIs, by intensifying glucose uptake and reducing plasma glucose, may play a protective, antioxidative role in hyperglycemic subjects.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme inhibitors reduce oxidative stress intensity in hyperglicemic conditions in rats independently from bradykinin receptor inhibitors

et al. 2016

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AimTo investigate whether bradykinin-independent antioxidative effects of angiotensin-converting enzyme inhibitors (ACEIs) exist in acute hyperglycemia.MethodsMale Wistar rats were divided into the normoglycemic group (n = 40) and the hyperglycemic group (n = 40). Hyperglycemia was induced by a single intraperitoneal injection of streptozotocin (STZ, 65 mg/kg body weight) dissolved in 0.1 mol/L citrate buffer (pH 4.5) 72 hours before sacrifice. The normoglycemic group received the same volume of citrate buffer. Each group was divided into five subgroups (n = 8): control group, captopril group, captopril + bradykinin B1 and B2 receptor antagonists group, enalapril group, and enalapril + bradykinin B1 and B2 receptor antagonists group. Captopril, enalapril, B1 and B2 receptor antagonists, or 0.15 mol/L NaCl were given at 2 and 1 hour before sacrifice. Oxidative status was determined by measuring the concentration of malondialdehyde and H2O2, and the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx).ResultsIn STZ-induced hyperglycemic rats ACEIs significantly reduced H2O2 and MDA concentration, while they significantly enhanced SOD and GPx activity. The hyperglycemic group treated simultaneously with ACEIs and bradykinin B1 and B2 receptor antagonists showed a significant decrease in H2O2 concentration compared to the control hyperglycemic group.ConclusionThese results suggest the existence of additional antioxidative effect of ACEIs in hyperglycemic conditions, which is not related to the bradykinin mediation and the structure of the drug molecule.

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“…Longer-term cell swelling might, however, be associated with pathological processes. In diabetesrelated conditions, cell swelling caused by exposure to high glucose is implicated in retinopathy (Wakisaka et al 1999). Volume regulation of pancreatic beta cells can also be induced by glucose (Best 1997) or osmotic changes (Britsch et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Glucose-inducible hypertrophy and suppression of anion efflux in rat beta cells

Chan

Saleh²,

Purje³

et al. 2002

Journal of Endocrinology

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Hypertrophy of beta cells from obese fa/fa rats is associated with increased sensitivity to basal glucose. Exposure to glucose in culture distorts insulin secretion more in beta cells from large than small islets from fa/fa rats. The aim of the present study is to investigate whether increased beta cell volume is associated with both glucose hypersensitivity and altered activity of the glucose-sensitive anion conductance. Beta cells from fa/fa rats had increased volume compared with those from lean rats after 24 h culture. Three-day exposure to 25 mM glucose in culture induced 10-15% hypertrophy in beta cells from lean rats and basal secretion from intact islets was increased tenfold. Estimates of ion channel activity were made from measurement of radiolabeled ion efflux. Taurine efflux, a marker of glucose-regulated anion channel activity, was reduced after high glucose exposure but no alterations in glucose-dependent K+ efflux were detected. The reverse hemolytic plaque assay was used to determine the contributions of the number of secreting cells (recruitment) versus secretion per cell in beta cells from enlarged (>250 microm diameter), intermediate (125-250 microm) and small (<125 microm) islets from lean and obese rats exposed to conditions mimicking hyperglycemia. After overnight culture, basal secretion was twofold greater from beta cells of large fa/fa islets compared with all other groups. Recruitment at low glucose was increased in all lean or fa/fa beta cells derived from >125 microm islets. When beta cells from small islets were exposed to supra-physiological glucose for 3 days, recruitment was increased at basal glucose and blunted at high glucose. Glucose exposure converts the recruitment profile of beta cells from small islets to resemble that of beta cells from large islets while inducing cellular hypertrophy and reduced anion conductance. However, hypertrophy alone did not predict functional characteristics of overnight-cultured beta cells from fa/fa rats.

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Suppression of Sodium-Dependent Glucose Uptake by Captopril Improves High-Glucose-Induced Morphological and Functional Changes of Cultured Bovine Retinal Pericytes

Cited by 21 publications

References 26 publications

Diabetic retinopathy

Diabetic retinopathy

Angiotensin-converting enzyme inhibitors reduce oxidative stress intensity in hyperglicemic conditions in rats independently from bradykinin receptor inhibitors

Glucose-inducible hypertrophy and suppression of anion efflux in rat beta cells

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