"Increased vascular permeability

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Small blood vessels are lined by a single layer of endothelial cells.
In some tissues, these form a complete layer of uniform thickness
around the vessel wall, while in other tissues there are areas of
endothelial cell thinning, known as fenestrations. The walls of small
blood vessels act as a microfilter, allowing the passage of water and
solutes but blocking that of large molecules and cells . Oxygen, carbon
dioxide and some nutrients transfer across the wall by diffusion, but
the main transfer of fluid and solutes is by ultrafiltration, as
described by Starling. The high colloid osmotic pressure inside the
vessel, due to plasma proteins, favours fluid return to the vascular
compartment. Under normal circumstances, high hydrostatic pressure at
the arteriolar end of capillaries forces fluid out into the
extravascular space, but this fluid returns into the capillaries at
their venous end, where hydrostatic pressure is low. In acute
inflammation, however, not only is capillary hydrostatic pressure
increased, but there is also escape of plasma proteins into the
extravascular space, increasing the colloid osmotic pressure there.
Consequently, much more fluid leaves the vessels than is returned to
them. The net escape of protein-rich fluid is called exudation; hence,
the fluid is called the fluid exudate
http://medweb.bham.ac.uk/http/mod/3/1/a/permeability.html "

Hello,

Vascular permeability is related to allowing the passage of water and
solutes but blocking that of large molecules and cells. Any change or
defect in it can effect passage of many bio-substances to the
extravascular tissues. Vasoconstriction, vasodialation, damages to
vascular walls, gaps between cells to cells in vascular walls, cells
adhesions, inflammatory conditions, regulatory machemisms, medications
etc. can effect such vascular permeability resulting into abnormal
movement of bio-substances between vascular and extravascular
compartments. I have few questions:-

1. Can some abnormailities in  vascular permeability effect movements
of biosubstances in between vascular and extravascular compartments?

2. Can vasoconstriction cause such movements in lesser quantity of
bigger moleculaes , vaso-dilation opposite?

3. Can glucose, lipids, protiens and insulin molecules be considered as
bigger molecules in this respect and so their passage to extravascular
compartments be reduced due to vasoconstriction, contracted conditions,
vascular wall's cells size and their adhesions?

4. Can it cause hyper-such biosubstances which can't be passed due to
decreased   vascular permeability, hyperglycemia, insulin resistance
etc?

5. Can unstability bio-substances in blood, blood tonicity/viscosity
effect vascular permeability?

6. Whether heat and cold, quantity of water intake, contracted or
relaxed conditions of vascular wall muscles, pH etc. can effect
vascular permeability?

Best wishes.