Increased levels of atherosclerosis markers in 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.
Larrousse
Maria
M
Hypertension Unit, Department of Internal Medicine, Hospital Clínic, Villaroel 170, 08036 Barcelona, Spain.
Bragulat
Ernesto
E
Segarra
Marta
M
Sierra
Cristina
C
Coca
Antonio
A
de La Sierra
Alejandro
A
D000328:Adult; D050197:Atherosclerosis / Q000097:blood* / Q000175:diagnosis* / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000503:physiopathology; D015815:Cell Adhesion Molecules / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood; D017364:Collagenases / Q000097:blood; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012982:Sodium, Dietary / Q000494:pharmacology*; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000097:blood
D015415:Biomarkers; D015815:Cell Adhesion Molecules; D018932:Chemokine CCL2; D015850:Interleukin-6; D012982:Sodium, Dietary; D019715:Tissue Inhibitor of Metalloproteinase-1; D002097:C-Reactive Protein; D017364:Collagenases