Fig. 3

PDE inhibition reveals predominant PDE2a activity in GECs and PDE3 & PDE5 activity in podocytes. Acute kidney slices from (a) Tie2:Cre/cGi500 mice or (c) Pod:Cre/cGi500 mice were superfused for 370 s with 50 µM BAY 60-7550, 250 µM Cilostamide, 250 µM Roflumilast, 250 µM Avanafil or 100 µM PF-04449613. The primarily inhibited PDE isoform is stated in brackets. Baseline-normalized FRET (CFP/YFP) ratios (R/Ro) of all analyzed glomeruli were calculated. (b, d) Time-lapse recordings display a sustained cGMP response after BAY 60-7550 and Cilostamide administration in GECs (b), whereas Cilostamide and Avanafil lead to a transient cGMP response in podocytes (d). Scattered bar plots display the maximal ∆R/Ro response for each compound during the entire measurement period of 1500 s. Data represent mean ± SEM of at least 8 glomeruli per condition obtained from slices of nine Tie2:Cre/cGi500 mice and six Pod:Cre/cGi500 mice.