ACE inhibition attenuates uremia-induced aortic valve thickening in a novel mouse model

ACE inhibition attenuates uremia-induced aortic valve thickening in a novel mouse model

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Abstract Background We examined whether impaired renal function causes thickening of the aortic valve leaflets in hyperlipidemic apoE-knockout (apoE-/-) mice, and whether the putative effect on the aortic valves could be prevented by inhibiting the angiotensin-converting enzyme (ACE) with enalapril.Methods Thickening of the cga 200 to cga 510 adapter aortic valve leaflets in apoE-/- mice was induced by producing mild or moderate chronic renal failure resulting from unilateral nephrectomy (1/2 NX, n = 18) or subtotal nephrectomy (5/6 NX, n = 22), respectively.Additionally, the 5/6 NX mice were randomized to no treatment (n = 8) or enalapril treatment (n = 13).The maximal thickness of each leaflet was measured from histological sections of the aortic roots.

Results Leaflet thickness was significantly greater in the 5/6 NX mice than in the 1/2 NX mice (P = 0.030) or the unoperated mice (P = 0.003).The 5/6 NX mice treated with enalapril had significantly thinner leaflets than did the untreated 5/6 NX mice (P = 0.

014).Conclusion Moderate uremia causes thickening of the aortic valves in apoE-/- mice, which can be attenuated by ACE inhibition.The nephrectomized apoE-/- mouse constitutes a berkley power worm 100 pack new model for investigating the mechanisms of uremia-induced aortic valve disease, and also provides an opportunity to study its pharmacologic prevention.