What is really going on with POTS? Is it a neurological disorder, a cardiac disorder?
Probably neither, the answer may lie within the purview of endocrinology?
There is a genetic component. This is clear. For example, patients with hypermobile joints are more likely to develop POTS.
Nobody knows what causes POTS. Apparently 10 different theories have been proposed. It is not due to direct dysfunction of sympathetic and parasympathetic nerves. It is not due to nerve damage such as what you might find in diabetic autonomic neuropathy.
Autonomic neuropathy should not be confused with dysautonomia. The two are quite different.
The prevailing explanation, according to a recent review, primarily relates POTS to dysfunction of the RAS. This stands for renin angiotensin system. Receptors for angiotensin may be off kilter. Angiotensin is messenger molecule or hormone known to be associated with the regulation of blood pressure, constriction of blood vessels and retention of salt and water. This what I remember from physiology. It turns out that Angiotensin and its associated receptors have wide reaches effects in a wide array of organs and organ systems– including the cardiovascular and nervous systems.
So, POTS is an endocrine disorder which may or may not be associated with genetic factors. It has overlap with other specialties including neurology and cardiology.
Drugs currently prescribed, including Fludrocortisone, DDAVP and Midodrine directly counter aberrant physiology associated with the disorder as viewed through this lens.