How can the effects of histamine lead to oedema?

Hi, I'm doing pharmacy and on a previous lecture on inflammation, it basically says that vasodilation (e.g. by histamine), works via NO to cause vasodilation and thus increased permeability of the blood vessels (I assume this just meant that having the blood vessels stretched more would make them thinner and so easier for materials to pass through), and thus can lead to oedema by there being an excess of fluid into the tissue space. This I can understand.

However, on the next lecture it says this:
"Actions of histamine
-H1 PLC linked to Ca++ elevation
-Vasodilator (arterioles) via nitric oxide
-Increased vascular permeability via endothelial contraction OEDEMA"

Isn't it the dilation, not contraction that causes the increased vascular permeability (and thus oedema)? And if it is by contraction, how does this occur when NO is released, which is a vasodilator?

Thanks for the help in advance

http://www.ncbi.nlm.nih.gov/books/NBK57148/

I recommend reading this chapter.

There are two pathways by which materials can be exchanged between the blood and the tissues: transcellular (through endothelial cells) and paracellular (between endothelial cells). When there is inflammation, histamine is released which causes vasodilation as it transiently up-regulates the expression of endothelial nitric oxide synthase, an enzyme which produces NO, hence more NO is produced. Histamine also causes endothelial cells themselves to contract/retract which causes the spaces between endothelial cells (interendothelial clefts) to become larger which increases vascular permeability - causing water and small solutes to enter the tissues leading to odema.

However, I think you might be confused as to what vasodilation is. Vasodilation is when smooth muscle found in the walls of arteries and especially arterioles relax, causing the diameter of the lumen to increase. Vasodilation does not refer to the stretching of endothelial cells. The reason for increased vascular permeability (and hence odema) is not because endothelial cells are being stretched out, it is because histamine as well as pro-inflammatory cytokines (such as TNF-α) causes endothelial cells to contract which increases the size of interendothelial clefts.

Ahh thank you SO much!! This has helped a lot thanks I did actually read about the transcellular/paracellular pathways but it was in another unit and didn't even think of this link so thank you, it's really helped with the bigger picture.
Haha thanks for picking up on my confusion there xD You're right that is what I thought, but I think I mostly get it now. ....But, just to clarify, vasodilation (of the arterioles) and constriction (of the endothelial cells) both are to serve the purpose of allowing more tissue fluid in which contains the mediators needed to repair the damage?

That's right. Histamine induces vasodilation which increases blood flow to the site of inflammation, bringing leucocytes with it. Histamine also causes endothelial cells to retract which increases the size of interendothelial clefts, allowing fluid rich with leucocytes to move into the tissues - a process known as diapedesis.