ArticleCardiovascular diabetology2011
Protein kinase C inhibition ameliorates functional endothelial insulin resistance and vascular smooth muscle cell hypersensitivity to insulin in diabetic hypertensive rats.
Article in Cardiovascular diabetology, 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, 27 citations in OpenAlex.
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- Review
- Relationship between early-onset stroke and triglyceride-glucose index among young Chinese adults.Lipids in health and disease · 2023Article
- [Experimental measurement and modeling analysis of active and passive mechanical properties of arterial vessel wall].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2020Article
- Role of oxidative stress in endothelial insulin resistance.World journal of diabetes · 2015Review
- Vascular dysfunction associated with type 2 diabetes and Alzheimer's disease: a potential etiological linkage.Medical science monitor basic research · 2014Review
- Biaxial vasoactivity of porcine coronary artery.American journal of physiology. Heart and circulatory physiology · 2012Article
- The link between metabolic abnormalities and endothelial dysfunction in type 2 diabetes: an update.Basic research in cardiology · 2012Review
- Article
- Role of PKC and CaV1.2 in detrusor overactivity in a model of obesity associated with insulin resistance in mice.PloS one · 2012Article
- Endothelial dysfunction in diabetes: pathogenesis, significance, and treatment.The review of diabetic studies : RDSReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveInsulin resistance, diabetes, and hypertension are considered elements of metabolic syndrome which is associated with vascular dysfunction. We investigated whether inhibition of protein kinase C (PKC) would affect vascular function in diabetic hypertensive (DH) rats.
methodsA combination of type 2 diabetes and arterial hypertension was produced in male Sprague Dawley rats by intrauterine protein deprivation (IUPD) followed by high salt diet. At the age of 32 weeks, DH rats were treated for 2 weeks with the angiotensin-converting enzyme inhibitor captopril (Capto, 30 mg/kg), PKC inhibitor ruboxistaurin (RBX, 50 mg/kg) or vehicle (n = 8 per group) and blood pressure was monitored using telemetry. At the end of experiments, femoral arteries were dissected, and vascular reactivity was evaluated with isovolumic myography.
resultsThe IUPD followed by high salt diet resulted in significant elevation of plasma glucose, plasma insulin, and blood pressure. Endothelium-dependent vascular relaxation in response to acetylcholine was blunted while vascular contraction in response to phenylephrine was enhanced in the DH rats. Neither Capto nor RBX restored endothelium-dependent vascular relaxation while both suppressed vascular contraction. Ex-vivo incubation of femoral arteries from control rats with insulin induced dose-response vasorelaxation while insulin failed to induce vasorelaxation in the DH rat arteries. In the control arteries treated with endothelial nitric oxide synthase inhibitor L-NAME, insulin induced vasoconstriction that was exacerbated in DH rats. Capto and RBX partially inhibited insulin-stimulated vascular contraction.
conclusionThese findings suggest that PKC inhibition ameliorates functional endothelial insulin resistance and smooth muscle cell hypersensitivity to insulin, but does not restore acetylcholine-activated endothelium-dependent vasodilation in DH rats.
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