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Abstract
The present work aimed mainly to illustrate:
1- The effect of a)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 NOχ Kidney tissues: Glutathione (GSH), superoxide dismutase (SOD), MDA, total DNA and RNA.