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Updated: Jul 7, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

Thiazide diuretics, endothelial function, and vascular oxidative stress.

Ming-Sheng Zhou¹, Ivonne Hernandez Schulman, Edgar A Jaimes

¹Nephrology and Hypertension Section, Veterans Affairs Medical Center, Miami, Florida 33125, USA.

Journal of Hypertension

|February 28, 2008

Summary

Thiazide diuretics lower blood pressure but do not reduce oxidative stress or improve endothelial function in hypertension models. These findings suggest their cardiovascular benefits may be limited to blood pressure reduction alone.

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Assessment of Vascular Function in Patients With Chronic Kidney Disease

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Published on: April 27, 2016

Area of Science:

Cardiovascular research
Pharmacology
Hypertension research

Background:

Hypertension is linked to increased oxidative stress and reduced nitric oxide bioactivity, involving monocyte chemoattractant protein (MCP)-1 and lectin-like oxidized low-density lipoprotein receptor (LOX)-1, contributing to atherogenesis.
The potential vasculoprotective effects of thiazide diuretics beyond blood pressure reduction remain to be fully elucidated.

Purpose of the Study:

To investigate whether the cardiovascular benefits of thiazide diuretics are solely due to blood pressure reduction or include independent pleiotropic vasculoprotective effects.
To assess the impact of thiazide diuretics on oxidative stress, endothelial function, and pro-atherogenic molecule expression in a hypertension model.

Main Methods:

Dahl salt-sensitive (DSS) rats were fed normal salt, high salt, or high salt with hydrochlorothiazide or chlorthalidone for 6 weeks.
Measurements included systolic blood pressure (SBP), left ventricular hypertrophy (LVH), proteinuria, aortic superoxide anion (O2(-)) production, endothelium-dependent relaxation (EDR), and expression of angiotensin II type 1 (AT1) receptor, LOX-1, and MCP-1.

Main Results:

High salt diet induced hypertension, LVH, proteinuria, increased aortic O2(-) production, impaired EDR, and upregulated AT1 receptor, LOX-1, and MCP-1.
Thiazide diuretics (hydrochlorothiazide, chlorthalidone) reduced SBP, LVH, and proteinuria.
However, thiazides did not decrease O2(-) production, AT1 receptor, LOX-1, or MCP-1 expression, nor did they improve EDR.

Conclusions:

Thiazide diuretics do not mitigate oxidative stress, enhance endothelial function, or downregulate pro-atherogenic molecules in this hypertension model.
The long-term cardiovascular protection offered by thiazide diuretics may be primarily attributed to their blood pressure-lowering effects.