Receptor | Ang II | Losartan | ||
---|---|---|---|---|
EC50 | Fmut | EC50 | Fmut | |
nM | nM | |||
Wild-type | ||||
hAT1 | 4.5 ± 0.6 | 1.0 | 15 ± 2.4 | 1.0 |
gAT1B | 3.3 ± 0.4 | 0.7 | 567 ± 54 | 38 |
gAT1B variants: gain-of-function | ||||
G107S | 4.1 ± 0.4 | 0.9 | 192 ± 21 | 13 |
V151I | 2.4 ± 0.5 | 0.5 | 557 ± 69 | 37 |
M195L | 6.6 ± 0.9 | 1.5 | 155 ± 19 | 10 |
G107S/V151I | 2.9 ± 0.5 | 0.6 | 156 ± 30 | 10.4 |
G107S/M195L | 4.3 ± 0.4 | 1.0 | 43 ± 2.5 | 2.9 |
Data are the mean ± S.E.M. obtained from two to four experiments (each done in triplicate) after displacement of125I-Sar1-Ang II binding. by increasing concentrations of losartan, for selected gAT1B mutant receptors transfected to COS-7 cells. To makeF mut values comparable, theF mut values of each mutant used the human EC50 value as a control for comparison.
F mut, mutant EC50/hAT1 EC50.