Arterial wall hypertrophy is ameliorated by α2-adrenergic receptor antagonist or aliskiren in kidneys of angiotensinogen-knockout mice

ConclusionsAlpha2-AR signaling is one of the causes of persistent renal arterial hypertrophy inAtg−/− mice. Aliskiren also angiotensinogen-independently reduces the extent of renal arterial hypertrophy, partly thorough downregulation of α2-ARs. Although renal arterial hypertrophy inAtg−/− mice appears to be of multifactorial origin, TGF- β1 may play a key role in the persistence of such hypertrophy.
Source: Clinical and Experimental Nephrology - Category: Urology & Nephrology Source Type: research