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Increased levels of atherosclerosis markers in salt-sensitive hypertension
Maria Larrousse1, Ernesto Bragulat, Marta Segarra
1Hypertension Unit, Department of Internal Medicine, Hospital Clínic, Villaroel 170, 08036 Barcelona, Spain.
Insights
Salt-sensitive hypertension is linked to higher inflammation markers like selectins and chemokines, and impaired blood vessel function. These changes may explain increased cardiovascular risk in these patients.
Area of Science:
- Cardiovascular Medicine
- Hypertension Research
- Endothelial Function Studies
Background:
- Salt sensitivity in essential hypertension is a known risk factor for endothelial dysfunction and cardiovascular events.
- Understanding the molecular markers associated with salt sensitivity is crucial for risk stratification and targeted therapies.
Purpose of the Study:
- To investigate serum markers of atherosclerosis and endothelial function in salt-sensitive versus salt-resistant hypertensive patients.
- To correlate these markers with salt intake and blood pressure responses.
Main Methods:
- Classified 43 hypertensive patients into salt-sensitive (n=20) and salt-resistant (n=23) groups based on 24-h blood pressure response to low and high salt diets.
- Assessed endothelium-dependent and independent vasodilation.
- Measured serum levels of inflammatory markers (CRP, sICAM-1, sVCAM-1, selectins, IL-6, MCP-1), matrix metalloproteinases (MMP-1, -2, -9), and tissue inhibitor of metalloproteinases (TIMP-1).
Main Results:
- Salt-sensitive hypertensives exhibited significantly higher levels of p-selectin, e-selectin, and monocyte chemotactic protein-1 (MCP-1) compared to salt-resistant individuals.
- Reduced serum levels of matrix metalloproteinase-9 (MMP-9) and increased tissue inhibitor of metalloproteinases-1 (TIMP-1) were observed in salt-sensitive patients.
- Endothelium-dependent vasodilation was significantly impaired in salt-sensitive hypertensives.
Conclusions:
- Salt-sensitive hypertension is characterized by distinct alterations in inflammatory markers (selectins, chemokines) and vascular remodeling proteins (MMP-9, TIMP-1).
- Impaired endothelium-dependent vasodilation is a key feature of salt sensitivity.
- These molecular and functional changes may underlie the increased target organ damage and cardiovascular risk associated with salt-sensitive hypertension.
Background:
Salt sensitivity in essential hypertension is associated with both endothelial dysfunction and increased cardiovascular risk. We evaluated several serum markers of atherosclerosis and endothelial function in a group of essential hypertensive patients classified on the basis of their salt sensitivity.
Methods:
Forty-three patients were classified as having salt-sensitive (20 subjects) or salt-resistant (23 subjects) hypertension on the basis of their 24-h blood pressure (BP) response from low salt (50 mmol/d) to high salt (250 mmol/d) intake. Endothelium-dependent and independent responses were measured in the forearm previously to salt manipulation. High-sensitivity C-reactive protein (CRP), soluble intercellular adhesion molecule type 1 (sICAM-1), soluble vascular cell adhesion molecule type 1 (sVCAM-1), e-selectin, p-selectin, interleukin-6 (IL-6), monocyte chemotactic protein type 1 (MCP-1), matrix metalloproteinases types 1, 2, and 9 (MMP-1, MMP-2, and MMP-9), and the tissue inhibitor of metalloproteinases type 1 (TIMP-1) were measured in serum on the last day of both low salt and high salt intakes.
Results:
Compared to salt-resistant patients, salt-sensitive hypertensives showed age-adjusted increased levels of p-selectin (P = .006), e-selectin (P = .042), and MCP-1 (P = .036), although differences in e-selectin were not maintained after adjustment for BP values. Moreover, salt-sensitive subjects exhibited decreased serum levels of MMP-9 (P = .007) and increased levels of TIMP-1 (P = .045). No differences in serum CRP, sICAM-1, sVCAM-1, or IL-6 were observed between salt-sensitive and salt-resistant patients. Finally, maximal acetylcholine-induced vasodilation (319% +/- 153% v 414% +/- 178% increase in forearm blood flow; P = .022 age-adjusted) was significantly impaired in salt-sensitive hypertensives.
Conclusions:
Serum markers of inflammation, especially selectins and chemokines, as well as markers of vascular remodeling, and endothelium-dependent vasodilation are altered in salt-sensitive hypertension. These alterations could help to explain the greater target organ damage and cardiovascular risk observed in salt-sensitive subjects.
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