I think it's because in Conn's you have aldosterone escape - once the arterial volume increases 15% or so, you have pressure induced natriuresis that causes loss of water and sodium and stabilizes the BP at a somewhat elevated level, but it is stabilized, so the system will adapt to the new higher set point - ie. the HR or TPR will decrease to try to normalize the BP as much as possible.
In a secondary hyperaldosteronism, I think you're seeing the heart or some part of the system fail and that's what's leading to the edema, and as mentioned above the aldosterone is just a maladaptive compensation.
Just hypothesizing...