Increased levels of atherosclerosis markers in salt-sensitive hypertension

M Larrousse, E Bragulat, M Segarra… - American journal of …, 2006 - academic.oup.com
M Larrousse, E Bragulat, M Segarra, C Sierra, A Coca, A de La Sierra
American journal of hypertension, 2006academic.oup.com
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 …
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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