Does sympathetic innervation cause vasodilation or vasoconstriction of uveal blood vessels?

Sympathetic innervation primarily causes vasoconstriction of the uveal blood vessels. This is due to the release of norepinephrine, which acts on alpha-adrenergic receptors located on the vascular smooth muscle of these vessels. When norepinephrine binds to these receptors, it results in the contraction of the smooth muscle, thereby narrowing the blood vessels and reducing blood flow—this condition is known as vasoconstriction.

In the context of ocular physiology, this process plays a role in regulating intraocular pressure and controlling blood supply to the iris and ciliary body. During times of stress or "fight or flight" responses, sympathetic activation helps redirect blood flow to essential systems, which is crucial for overall bodily function.

Other choices are less relevant in this context. For example, vasodilation typically involves parasympathetic stimulation or certain local factors, while the "no effect" option does not account for the established relationship between sympathetic activity and vascular control. Increased permeability does not directly correlate with vasomotor tone regarding blood vessel contraction or dilation. Thus, understanding the action of sympathetic innervation in relation to uveal blood vessels is fundamental to this topic.