However, low-level n-VNS has improved POTS-like symptoms in rabbit models.6,7 Specifically, the rabbit models had auto-antibodies to the muscarinic acetylcholine receptor M2, α1-adrenergic receptor, or the β1-adrenergic receptor.6,7 Following 2–4 weeks of daily vagal nerve stimulation, the rabbits had decreased postural tachycardia and variability in HR.6,7 It is theorized that the increase in acetylcholine from vagus nerve stimulation improved the rabbit POTS symptoms by increasing parasympathetic activity enough to overcome the auto-antibody–induced increased sympathetic activity.6 This evidence concerns the gene CHRM2 and postural orthostatic tachycardia syndrome.