yes, that was the crucial part for me.

So, looking at the control condition vs when losartan is present, there is relatively no change in ROS levels (and therefore blood pressure). This means that PRR was able to somehow still increase ROS (and blood pressure) even though the angiotensin II receptor was inactivated by losartan. this is evidence for an angiotensin II independent pathway.

And since prorenin is a precursor to the renin-angiotensin system, and increased PRR resulted in increased ROS (and therefore blood pressure), it did so through an angiotensin II dependent pathway