Association between systemic microvascular dysfunction and resistant hypertension: Insights from a clinical
Vinicius Crahim1, Valéria Verri1, Andrea De Lorenzo1
1National Institute of Cardiology, Rio de Janeiro, Brazil.
Microvascular Research
|March 15, 2026
Summary
Resistant arterial hypertension (RAH) shows significant systemic microvascular impairment affecting endothelial function and structure. Non-resistant arterial hypertension (NRAH) also exhibits microvascular dysfunction compared to healthy controls.
Area of Science:
- Cardiovascular Science
- Hypertension Research
- Microvascular Physiology
Background:
- Resistant arterial hypertension (RAH) is linked to high cardiovascular risk, potentially due to systemic microvascular dysfunction.
- While non-resistant arterial hypertension (NRAH) shows early endothelial impairment, direct microvascular comparisons across RAH, NRAH, and controls are limited.
Purpose of the Study:
- To compare systemic microvascular function in patients with RAH, NRAH, and normotensive individuals.
- Utilize laser speckle contrast imaging to assess microvascular reactivity.
Main Methods:
- Assessed microvascular reactivity using acetylcholine (ACh) and sodium nitroprusside (SNP) iontophoresis, and post-occlusive reactive hyperemia (PORH).
- Compared baseline microvascular conductance, vasodilation responses (AUCs for ACh and SNP), and PORH parameters via one-way ANOVA.
Main Results:
- Baseline microvascular conductance was higher in controls than hypertensive groups.
- Endothelium-dependent vasodilation (ACh AUC) and endothelium-independent vasodilation (SNP AUC) were progressively impaired from controls to NRAH to RAH.
- RAH showed reduced peak microvascular conductance and smaller delta values during PORH, indicating structural arteriolar issues.
Conclusions:
- RAH is characterized by significant systemic microvascular impairment impacting endothelial function and vascular structure.
- These microvascular alterations in RAH coexist with metabolic and renal disorders.
- Complex interactions between vascular, metabolic, and renal factors contribute to treatment-resistant hypertension.
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