Key result
Angiotensin II plus sodium overload exacerbates intrarenal TGF-β1, α-SMA, and NF-κB in rats independently of BP.
p-value: p=<0.01
Angiotensin II combined with acute sodium overload exacerbates intrarenal fibrotic and inflammatory markers independently of blood pressure in normal rats.
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Should not alter clinical practice; leaves open whether Ang II–sodium interactions drive human renal fibrosis.
Rosón et al. (2008) studied Sodium overload. Angiotensin II and sodium overload vs. Isotonic saline solution (NaCl 0.15 mol/L) was evaluated on Intrarenal TGF-β1 immunostaining (p=<0.01). The interaction of Angiotensin II with acute sodium overload exacerbated intrarenal TGF-β1, α-SMA, and NF-κB expression independently of blood pressure changes in normal rats.