<span class="center-menu">← <small>PREVIOUS: [[4.3. Neuroendocrine dysregulation]]</small> | <small>NEXT: [[4.5. Small fiber neuropathy and nerve dysfunction]]</small> →</span> -------- ##### Summary >[!Summary] >- the presence of α1 adrenergic receptor (AR) autoantibodies acting as partial peripheral receptor antagonists could cause compensatory sympathetic activation to maintain adequate vasoconstriction, which could then induce tachycardia via β-ARs[[#^1]] >- β1-AR- and β2-AR-activating autoantibodies could also contribute to the tachycardia[[#^1]] -------- >*“Li et al. [57] presented evidence from two cohorts of POTS patients for α1 adrenergic receptor (AR) autoantibodies acting as partial peripheral receptor antagonists. Compensatory sympathetic activation to maintain adequate vasoconstriction could then induce tachycardia via β-ARs. β1-AR- and β2-AR-activating autoantibodies could also contribute to the tachycardia.” *<small>([[Garland-2015]], [p. 8](zotero://open-pdf/library/items/CAWTWYLR?page=8&annotation=LST8Y6QC))</small>^1