Role of SCTR/AT1aR heteromer in mediating ANGII-induced aldosterone secretion
Fig 2
SCTR potentiates ANGII-induced increase in [Ca2+]i.
(A) [Ca2+]i change in primary ZG cells obtained from C57 and SCTR-/- mice, in response to ANGII (ranging from 0.1 nM to 1 μM). ANGII dose-dependently increased [Ca2+]i in C57 ZG cells. The tested ANGII dosages lead to a minor increase in [Ca2+]i in SCTR-/-, similar to the 0.1 nM ANGII-treated ZG cells of C57 mice. The maximal ANGII-induced [Ca2+]i increase was recorded at around 9 min, 11 min and 12 min post-ANGII loading, depending on the dosage of ANGII. Loading buffer was loaded as negative control. *, P <0.05 vs 0.1 nM ANGII-treatment in corresponding genotype. #, P < 0.05, vs counterparts in C57 mice. Data are present as mean + SEM from at least five independent experiments. (B) Extracellular calcium is a prerequisite for ANGII-induced Ca2+ mobilization and is the major source of [Ca2+]i influx. Pre-exposure to EGTA (5 mM) prior to ANGII (10 nM) abolished extracellular Ca2+ mobilization in C57 ZG cells. In contrary, increased [Ca2+]i upon ANGII was observed, until EGTA was loaded. The [Ca2+]i influx induced by ANGII was gradually and eventually chelated by EGTA nearly back to the resting level. Data are present as mean ± SEM from three independent experiments.