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Title: Possible involvement of phosphatidylinositol 3 kinase in experimental vascular endothelium dysfunction
Researcher: Sharma, Saurabh
Guide(s): Manjeet Singh
Keywords: pharmacy
vascular endothelium
Endothelial Phenotypes
Upload Date: 17-May-2013
University: Punjab Technical University
Completed Date: 2012
Abstract: Vascular endothelium plays a role in capillary transport of nutrients and drugs and regulates angiogenesis, homeostasis, as well as vascular tone and permeability As a major regulator of local vascular homeostasis, the endothelium maintains the balance between vasodilatation and vasoconstriction, procoagulant and anticoagulant, prothrombotic and antithrombotic mechanisms. Diabetes mellitus causes the activation of aldose reductase, polyol pathway and advanced glycation-end-product formation that collectively affect the phosphorylation status and expression of endothelial nitric oxide synthatase (eNOS) and causes vascular endothelium dysfunction. Elevated homocysteine levels have been associated with increase in LDL oxidation, generation of hydrogen peroxides, superoxide anions that increased oxidative degradation of nitric oxide. Hyperhomocysteinemia has been reported to increase the endogenous competitive inhibitors of eNOS viz- L-N-monomethyl arginine (L-NMMA) and asymmetric dimethyl arginine (ADMA) that may contribute to vascular endothelial dysfunction. Hypercholesterolemia stimulates oxidation of LDL-cholesterol, release of endothelins, and generation of ROS. The increased cholesterol and triglyceride level and decreased protective HDL level, decreases the activity and expression of eNOS and disrupts the integrity of vascular endothelium, due to oxidative stress. Hypertension also stimulates release of endothelins, vasoconstrictor prostanoids, angiotensin II, inflammatory cytokines, xanthine oxidase and, thereby, reduces bioavailability of nitric oxide. Thus, the cellular and molecular mechanisms underlying diabetes mellitus, hyperhomocysteinemia, hypercholestrolemmia and hypertension leads to animbalance of phosphorylation and dephosphorylation status of lipid and protein kinase that cause modulation of vascular endothelial L-arginine/nitric oxide synthetase (eNOS), to produce vascular endothelium dysfunction.
Pagination: 145p.
Appears in Departments:Department of Pharmacy

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02_dedication.pdf284.44 kBAdobe PDFView/Open
03_declaration.pdf89.84 kBAdobe PDFView/Open
04_acknowledgement.pdf71.15 kBAdobe PDFView/Open
05_abstract.pdf69.42 kBAdobe PDFView/Open
06_table of contents.pdf39.62 kBAdobe PDFView/Open
07_list of abbreviations.pdf39.48 kBAdobe PDFView/Open
08_list of figures.pdf71.63 kBAdobe PDFView/Open
09_list of publications.pdf75.63 kBAdobe PDFView/Open
10_chapter 1.pdf47.82 kBAdobe PDFView/Open
11_chapter 2.pdf46.34 kBAdobe PDFView/Open
12_chapter 3.pdf409.7 kBAdobe PDFView/Open
13_chapter 4.pdf159.63 kBAdobe PDFView/Open
14_chapter 5.pdf1.84 MBAdobe PDFView/Open
15_chapter 6.pdf841.83 kBAdobe PDFView/Open
16_chapter 7.pdf57.43 kBAdobe PDFView/Open
17_chapter 8.pdf12.09 kBAdobe PDFView/Open

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