<span class="center-menu">← <small>PREVIOUS: [[4.2. Cardiovascular and hemodynamic abnormalities]]</small> | <small>NEXT: [[4.4. Immunological abnormalities]]</small> →</span> -------- ##### Summary >[!Summary] >- no statistically significant association was found between level of urinary sodium and level of plasma norepinephrine[[#^1]] >- 1 in 3 has hyperadrenergic features[[#^2]] >- subset of POTS patients demonstrate relative hypovolaemia and impaired renin-angiotensin-aldosterone regulation, which might be caused by neuroendocrine and renal dysfunction leading to chronic intravascular fluid deficiency[[#^3]] -------- >*“The heart rate increment to head-up tilt was not statistically significantly related to standing norepinephrine level (P=.40, Spearman ρ) or norepinephrine increment on standing (P=.19, Spearman ρ). No statistically significant correlation was found between 24-hour sodium excretion and norepinephrine increment on standing (P=.73, Spearman ρ). No statistically significant association was found between level of urinary sodium (<100, 100-149, ≥150 mEq/24 h) and level of plasma norepinephrine (≤600, >600 pg/mL)” *<small>([[Thieben-2007]], [p. 5](zotero://open-pdf/library/items/5WXWEQWX?page=5&annotation=JHJDBWBP))</small>^1 >*“1 in 3 has hyperadrenergic features,” *<small>([[Thieben-2007]], [p. 6](zotero://open-pdf/library/items/5WXWEQWX?page=6&annotation=RZWN3B43))</small>^2 >*“a subset of POTS patients demonstrate relative hypovolaemia and impaired renin-angiotensin-aldosterone regulation [54]. In these patients, POTS phenotype might be caused by neuroendocrine and renal dysfunction leading to chronic intravascular fluid deficiency.” *<small>([[Fedorowski-2019]], [p. 6](zotero://open-pdf/library/items/BZ35QDLR?page=6&annotation=MAVEDY4P))</small>^3