Which of the following is NOT a factor in the depolarization of the GI tract?

In the context of the gastrointestinal (GI) tract, depolarization primarily refers to the change in membrane potential that leads to the generation of action potentials in smooth muscle cells, facilitating contraction and motility.

Stretching of the gut wall activates mechanoreceptors, which can lead to depolarization through the release of neurotransmitters and hormones that promote muscle contractions. Acetylcholine is a key neurotransmitter in the autonomic nervous system associated with stimulation of digestive activity, promoting depolarization and contraction of GI smooth muscle. Specific gastrointestinal hormones also play an essential role in regulating motility and facilitating depolarization within the GI tract by modulating smooth muscle activity.

In contrast, sympathetic stimulation generally has an inhibitory effect on the GI tract. The sympathetic nervous system tends to reduce digestive activities, including motility, by releasing norepinephrine, which may hyperpolarize smooth muscle cells and decrease the likelihood of contraction. This makes sympathetic stimulation a non-contributory factor in the direct process of depolarization in the GI tract. Therefore, it is not associated with promoting depolarization like the other factors mentioned.