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editorial
. 2009 Oct 21;298(1):F37–F48. doi: 10.1152/ajprenal.00519.2009

Fig. 6.

Fig. 6.

Afferent arteriole average diameter responses (delta % of baseline) to ANG I (0, 1, 10, 100 nM) in the presence of AT1 receptor blockade (A; n = 6, 7), ACE inhibition (B; n = 6, 6), serine protease inhibition (C; n = 6, 6), or combined ACE and serine protease inhibition (D; n = 7, 6) in kidneys of control (□) and diabetic (·) mice. Afferent arteriole vasoconstriction produced by ANG I was significantly attenuated by AT1 receptor blockade, ACE inhibition, combined ACE and serine protease inhibition, but not by serine protease inhibition alone in kidneys of control mice. Afferent arteriole vasoconstriction produced by ANG I was significantly attenuated by AT1 receptor blockade, serine protease inhibition, and combined ACE and serine protease inhibition, but not by ACE inhibition alone in kidneys of diabetic mice. *P ≤ 0.05 vs. baseline diameter. †P ≤ 0.05 control vs. diabetic. #P ≤ 0.05 vs. ANG I alone.