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Trandolapril Hydrochloride is an antihypertensive. Angiotensin converting enzyme (ACE) inhibitor. | [in vivo]
Trandolapril hydrochloride (3 mg/kg/day; p.o.; 7 d) reduces renal fibrosis in obstructive nephropathy in mice, by inhibiting renal interstitial matrix expression and myofibroblast activation, decreasing renal proinflammatory cytokine RANTES and TNF-α level[2].
Trandolapril hydrochloride (0.3 mg/kg/day; p.o.; 4 weeks) improves arterial mechanics in rats, prevents arterial hypertrophy, collagen and cellular fibronectin accumulation[3].
randolapril (0.3 mg/kg/day; p.o.; 4 months) exhibits a chronic anti-hypertension effects in rats, results in blood pressure decreasing[3].
Trandolapril hydrochloride (0.25 mg/kg; p.o.; twice a day; 4 months) inhibits Atherosclerosis in the Watanabe Heritable Hyperlipidemic Rabbit[4].
Animal Model: | UUD (unilateral ureteral obstruction) model in Male CD-1 mice (18-22 g)[2] | Dosage: | 3 mg/kg | Administration: | Oral gavage; daily, for 7 days | Result: | Resulted in renal interstitial matrix expression (including fibronectin, type I, and type III collagen) decreasing, and inhibited myofibroblast activation by surprising a-smooth muscle actin (a-SMA) expression, decreased the RANTES (regulated on activation, normal T cell expressed and secreted) and TNF-α level.
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Animal Model: | SHR model (spontaneously hypertensive rats, 4-week-old)[3] | Dosage: | 0.3 mg/kg | Administration: | Oral gavage; daily for 4 weeks | Result: | Reduced collagen content in the aortic media and increased ariterial distensibility up to about 80%.
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Animal Model: | Watanabe heritable hyperlipidemic rabbit (3 months old)[4] | Dosage: | 0.25 mg/kg | Administration: | Oral gavage; twice a day; 9 months | Result: | Decreased in atherosclerotic involvement of the intimal surface, and also decreased cholesterol content in descending thoracic aorta.
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