Haemodynamic determinants of supine hypertension in patients with classical orthostatic hypotension

Amber H van der Stam1,2, Boriana S Gagaouzova2,3, Fabian I Kerkhof2

  • 1Radboud University Medical Center, Donders Institute for Brain, Cognition and Behavior, Department of Neurology, Center of Expertise for Parkinson & Movement Disorders, Nijmegen.

Journal of Hypertension
|November 13, 2025
PubMed

Insights

Classical orthostatic hypotension (cOH) patients exhibit high supine blood pressure due to elevated total peripheral resistance (TPR). This high TPR fails to increase upon standing, leading to orthostatic hypotension.

Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Function
  • Hypertension Research

Background:

  • The interplay between supine hypertension and classical orthostatic hypotension (cOH) remains poorly understood.
  • Investigating the determinants of blood pressure regulation in individuals with cOH is crucial for understanding cardiovascular pathophysiology.

Purpose of the Study:

  • To elucidate the relationship between classical orthostatic hypotension (cOH) and supine hypertension.
  • To determine the relative contributions of heart rate (HR), stroke volume (SV), and total peripheral resistance (TPR) to supine and upright blood pressure (BP).

Main Methods:

  • Retrospective analysis of tilt tests in normotensive controls, hypertensive controls, and cOH patients with (cOH/SH+) and without (cOH/SH-) supine hypertension.
  • Linear regression and logratio analysis were employed to assess the contributions of HR, SV, and TPR to BP regulation.
  • Hypertension defined as supine systolic blood pressure (SBP) ≥ 140 mmHg; P < 0.003 considered significant.

Main Results:

  • High supine SBP was consistently associated with elevated TPR in both patients and controls.
  • Orthostatic SBP decrease was more pronounced in cOH patients with higher supine SBP, primarily due to a failure of TPR to increase upon standing in the cOH/SH+ group.
  • Stroke volume (SV) contributed less to orthostatic BP changes in cOH/SH- compared to cOH/SH+, while heart rate (HR) contributions were similar across cOH groups.

Conclusions:

  • Elevated supine TPR is a key factor in supine hypertension within cOH patients.
  • The inability to adequately increase upright TPR significantly contributes to the orthostatic blood pressure fall in cOH.
  • While autonomic failure explains the BP drop, the persistent high supine TPR suggests a role for slow-acting vasoconstrictors in maintaining supine hypertension.
Abstract

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