If you REALLY want the answer, its a little long winded.
Let's back it up a little.
There are a couple of forces at work when it comes to fluid out of a capillary.
First You have the
Hydrostatic Capillary Pressure pushing fluid out into the interstitium and the
Hydrostatic Interstitial Pressure pushing fluid back into the capillary. The capillary hydrostatic pressure is usually stronger, this pushes fluid out.
Next you have the
oncotic capillary pressure pulling fluid into the capillary from the intersititum. These are osmoles like protein and red blood cells. The interstitium SHOULDNT have a whole lot of protein, so the
oncotic interstitial pressure pulling fluid out is negligible. The capillary hydrostatic pressure is usually stronger, pulling fluid in.
Overall, the hydrostatic capillary pressure pushing fluid out is stronger in the arterial side of the capillaries (pushing fluid out) and weaker on the venous side (which is why most fluid comes back into the venous system instead of causing edema). Your questions focuses on the arterial side.
Finally, there is the
permeability coefficient, K. The tigheter the endothelial cells are linked together, the less diffusion there can be. The wall is tighter. The looser they are connected the more fluid can move. "K is a Konstant" mathematically, but it can be changed, influenced by hormones and cytokines.
Maybe you remember this from physio?
Diffusion = K [(Pcap-Pinter) - (pcap - pinter)]
K goes up = more fluid shift (think the liver)
K goes down = less fluid shift (think the blood brain barrier)
In the case of ACE-inhibitors, excess bradykinin production in the lungs results in "vasodilation." But what it ACTUALLY MEANS is that the walls of the endothelium get looser.
K goes up. K goes towards 1. That means ALOT of fluid can now move. With hydrostatic capillary pressure winning the day, fluid leaks out into the interstitium, which both interferes with gas exchange and acts an irritant.
You cough.
Theoretically, switching from an ACE-inhibitor (works "in the lungs" where "Ang I is converted to Ang II") to an ARB (works "at the kidneys" where "Ang II activates the receptors") should eliminate the excess bradykinin, and with it, vasodilation, permeability, and fluid shifts into the interstitium
The summary "bradykinin's histamine-like activity" sums it up, but without understanding the fundamentals, other's reading this might miss what that means.