| Abstract: |
SUMMARY AND CONCLUSIONThe present work aimed mainly to illustrate:1- The effect ofa) RAAS activation, subsequent Ang II and aldosterone increase contributing to renal injury through progression of prothrombotic state.b) Mechanism of antihypertensive drugs to counteract RAAS activation in diabetic nephritic rats.2- Role of oxidative stress and free radical production regarding to development of salt sensitive hypertension induced venous thrombosis progression.First part: It delt with certain antihypertensive drugs, categorized as:1- Aldosterone antagonist (Aldactone)2- Angiotensin converting enzyme inhibitor (Primox)3- β-Blocker (Dilatrol)Second part: It delt with green tea extract (Catechin) as an example of natural antioxidant.Hemodynamic parameters:Blood pressure, heart rate and dry thrombus weight.Biochemical markers selected were:Whole blood: Electrolytes (Na+, K+).Serum: Glucose, fructosamine, creatinine, ACE, aldosterone, TGF-β1 and lipid profile.Plasma: susceptibility of non HDL-C to oxidation, renin activity and PAI-1.Urine: Urinary NOχKidney tissues: Glutathione (GSH), superoxide dismutase (SOD), MDA, total DNA and RNA.Histological study: Using two types of examination:A- LM type: Using hematoxylin and eosin stain to illustrate tubular injury, cellular vacuolization, vascularity and degree of necrosis.B- EM type: An electron micrograph from a section in the renal cortex to study changes in glomerulus.Experimental design: It included two parts:The first part:One week after acclimatization, the rats were divided into 2 groups, the first one was fed on high salt diet (4% NaCl), and the second one received low salt diet (0.08% NaCl). Nω-nitro-L-arginine methyl ester (L-NAME, 0.1 mg/ml) was provided to all animals in their drinking water for two weeks. Induction of diabetes was done through i.p. injection of alloxan (150 mg/kg). Animals achieved serum glucose level ≥200 mg/dl and creatinine level >1.5 mg/dl were recruited for the study.
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