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. Author manuscript; available in PMC: 2009 Dec 1.
Published in final edited form as: J Hypertens. 2008 Dec;26(12):2414–2425. doi: 10.1097/HJH.0b013e328312c86a

Fig. 2.

Fig. 2

Inhibition of NKA from pig renal outer medulla by MBG (a) and effect of 3E9 and 4G4 anti-MBG mAbs on MBG-induced inhibition of NKA from pig kidney (b). Inhibition of NKA from rat renal medulla by MBG (c), and effect of 3E9 anti-MBG mAb on MBG-induced inhibition of NKA from rat renal medulla (d). Concentration-response curves were determined five to eight times. These were averaged to give means SEM. In pig renal medulla, the fit of the curve converged with inhibition occurring at the levels of low-affinity binding only (IC50 = 0.46 ± 0.23 μmol/l). In rat renal medulla, the fit of the curve converged with inhibition occurring at the level of higher-affinity and lower-affinity binding sites (IC50 = 1.9 ± 1.3 nmol/l and 4.3 ± 2.9 μmol/l, respectively). Each bar represents means ± SEM from five measurements. By one-way ANOVA followed by Newman–Keuls test: *P < 0.05; **P < 0.01 vs. effect of MBG. NKA, Na/K-ATPase; mAb, monoclonal anti-marinobufagenin antibody; MBG, marinobufagenin.