Notice that A) Bronchoconstriction, B) Glandular secretion, D) Peristalsis, E) Vasodilation of skin are all under parasympathetic control.
The only sympathetic control is heart rate, which would increase.
The way I excluded vasodilation was this: the sympathetic receptor that dilates is ฮฒ2, which is not stimulated by norepinephrine. So to stimulate the receptor, the stellate ganglion would have had to first stimulate the adrenal medulla to release epinephrine (stellate too high to stimulate the medulla).
I incorrectly chose vasodilation. Found out that itโs actually vasoconstriction (vasodilation is parasympathetic):
Autonomic nerve fibers are also crucially involved in the regulation of vascular effects in the skin. Sympathetic nerve fibers release norepinephrine and/or NPY to innervate arterioles, arteriovenous anastomoses, and venous sinusoids which results in vasoconstriction, whereas parasympathetic nerves mediate vasodilatation through activation of venous sinusoides by the release of ACh and VIP/peptide histidine methionine.
https://physiology.org/doi/full/10.1152/physrev.00026.2005
I thought that the primary sympathetic innervation to the heart was through T1-T4. Why would stimulation of this ganglion not affect skin vessels in the upper limb?
the stellate ganglion is part of the sympathetic nervous system flight or fight. Increase heart rate is the most obvious.
submitted by โseagull(1933)
So, T1/2-T5/6 are the sympathetic level for the heart. The stellate ganglion are cervical sympathetic ganglion. This question seems more incorrect (or a huge leap) to me. But hey, I know people will disagree.