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Published on: October 15, 2010
Serum Markers of Endothelial Dysfunction and Inflammation Increase in Hypertension with Prediabetes Mellitus
Zhouqing Huang1, Chen Chen1, Sheng Li1
1Department of Cardiology, The Key Lab of Cardiovascular Disease of Wenzhou, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou, P.R. China .
Insights
Hypertension and prediabetes significantly increase inflammation and endothelial dysfunction markers. The combination of both conditions further elevates intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-α), worsening these effects.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Immunology
Background:
- Hypertension and prediabetes are prevalent conditions associated with increased cardiovascular risk.
- Endothelial dysfunction and chronic inflammation are key pathophysiological mechanisms in these diseases.
Purpose of the Study:
- To investigate endothelial dysfunction and inflammation in patients with hypertension and prediabetes.
- To analyze the levels of specific adhesion molecules and inflammatory factors in different patient groups.
Main Methods:
- A study involving 133 outpatients categorized into control, hypertension-only, and hypertension with prediabetes groups.
- Enzyme-linked immunosorbent assay (ELISA) was used to measure plasma concentrations of ICAM-1, TNF-α, P-selectin, and IL-6.
Main Results:
- Patients with hypertension (H) and hypertension with prediabetes (HD) showed significantly higher levels of all four biomarkers compared to controls (N).
- The HD group exhibited significantly higher levels of ICAM-1 and TNF-α compared to the H group.
- No significant differences in P-selectin and IL-6 levels were found between the H and HD groups.
Conclusions:
- Prediabetes and hypertension contribute to endothelial dysfunction and inflammation by increasing soluble adhesion molecules and inflammatory cytokines.
- The comorbidity of hypertension and prediabetes exacerbates inflammation and endothelial dysfunction, particularly through enhanced ICAM-1 and TNF-α expression.
Aims:
The aim of this study was to examine endothelial dysfunction and inflammation in hypertension and prediabetes by studying adhesion molecules and inflammatory factors.
Methods And Results:
This study included 133 outpatients. Participants were categorized into three groups based on the presence or absence of hypertension and prediabetes: control subjects without prediabetes and hypertension (N group, n = 39); patients with hypertension only (H group, n = 34); and patients with hypertension and prediabetes (HD group, n = 60). Hypertension was diagnosed according to JNC7 criteria. Prediabetes was defined according to 2010 American Diabetes Association criteria. Plasma was isolated from overnight fasting blood samples for enzyme-linked immunosorbent assay (ELISA) analysis of concentrations of intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), P-selectin, and interleukin-6 (IL-6) as indicators of endothelial function and inflammation. We found that the H and HD groups showed significantly higher levels of all four biomarkers compared with the N group (all p < 0.01). The HD group also showed significantly higher levels of ICAM-1 (p = 0.042) and TNF-α (p < 0.01) compared with the H group; no significant differences in P-selectin (p = 0.59) and IL-6 (p = 0.70) levels were observed among these groups.
Conclusions:
Prediabetes and hypertension induce endothelial dysfunction and inflammation by elevating levels of soluble adhesion molecules and inflammatory cytokines. The comorbidity of these diseases may exacerbate inflammation and endothelial dysfunction by enhancing the expression of ICAM-1 and TNF-α.
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