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. 2018 Nov 14;316(2):F253–F262. doi: 10.1152/ajprenal.00491.2017

Fig. 9.

Fig. 9.

Inhibition of adenosine monophosphate kinase (AMPK) with Compound C (Comp C) did not change phosphorylation of aquaporin-2 (AQP2) at serine 261 in rat inner medulla (IM). A: representative Western blot showing AQP2 abundance and phosphorylated AQP2 in rat IM with hypertonic (Hyper) stimulation (690 mosmol/kgH2O) and treatment of 10 µM Compound C (AMPK inhibitor) for 15 min. Brackets indicate AQP2 glycosylated protein between 35 and 45 kDa and arrows indicate unglycosylated protein at 29 kDa. Samples from a different rat were loaded into each lane. B: bar graph showing the ratio of the band densities of phosphorylated AQP2 to total AQP2 abundance. Bars  = means ± SE; results were not significantly different between hypertonic treatment alone and combination of hypertonicity and Compound C; n = 4 rats/condition.