Elevated Levels of Circulating Cell Adhesion Molecules in Uncomplicated Essential Hypertension

Abstract

Elevated levels of circulating soluble cell adhesion molecules are associated with the development of cardiovascular disease. We tested the hypothesis that circulating levels of soluble cell adhesion molecules are elevated in older men with uncomplicated essential hypertension, which may contribute to the increased risk of atherosclerosis in this population. Circulating levels of soluble intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin were measured in 11 hypertensive (69+/-1 years) and ten normotensive (65+/-1 years) older men who were free of overt atherosclerotic disease, diabetes, and dyslipidemia. The hypertensive subjects had higher (P < .05) circulating levels of soluble intercellular adhesion molecule-1 (232.4+/-16.5 v 189.8+/-11.1 ng/mL) and vascular adhesion molecule-1 (737.3+/-65.6 v 565.7+/-46.8 ng/mL) compared with their normotensive peers. However, there was no difference in the levels of soluble E-selectin between the hypertensive (51.1+/-3.9 ng/ mL) and normotensive (48.8+/-6.6 ng/mL) subjects. Univariate analysis revealed a positive correlation between soluble intercellular adhesion molecule-1 and both systolic (r = 0.50, P = .02) and diastolic (r = 0.49, P = .03) blood pressure. In addition, soluble vascular adhesion molecule-1 was positively correlated with age (r = 0.60, P = .004) and systolic blood pressure (r = 0.43, P = .05). The results of this study support the hypothesis that circulating levels of soluble cell adhesion molecules are elevated in older men with uncomplicated essential hypertension.

Endothelial dysfunction is associated with increased levels of biomarkers in essential hypertension

“…6 Other inflammatory biomarkers, such as high-sensitivity C-reactive protein, soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule or interleukin-6 did not correlate with endothelial function in this group of patients. Although they are also produced totally or partially in the endothelium, and they have been found increased in hypertension 13,14 or in patients with cardiovascular disease, 21 no clear relationship with the endothelial function was observed in this study. A possible explanation of this different behaviour could be found in the relative young age of the study population, which was recently diagnosed of essential hypertension and was free from overt cardiovascular disease.…”

“…5,10,11 The impaired endothelial function is closely linked with increased oxidative stress, 11,12 inflammation, remodelling and atherogenesis. 9 In this view, several acute-phase reactants, soluble adhesion molecules, chemokines and metalloproteinases are altered in patients at risk of cardiovascular events, such as hypertensives, [13][14][15][16][17] diabetics 18 or those with left ventricular hypertrophy. 19,20 Moreover, in patients with coronary heart disease some of these serum markers have prognostic implications.…”

Biomarkers of inflammation and endothelial dysfunction as predictors of pulse pressure and incident hypertension in type 1 diabetes: a 20 year life-course study in an inception cohort

“…In addition, endothelial dysfunction/inflammation may lead to smooth muscle cell proliferation and increased synthesis of structural proteins such as collagen within the vascular wall, leading to structural stiffening of large arteries [3,9]. Previous studies on soluble CAMs and BP have produced contradictory findings but have been mostly cross-sectional and not focused on the pulsatile component of BP [44][45][46][47][48][49][50]. Appreciation of the BP curve as a summation of a steady component (MAP) and a pulsatile component (pulse pressure) has provided additional information in terms of CVD risk prediction to that traditionally obtained on the basis of elevated SBP and/or DBP alone [5].…”

Soluble integrin adhesion receptors and atherosclerosis: much heat and a little light?

“…22,36 As Rizzoni and colleagues report, many risk factors for atherosclerosis, including diabetes and hypertension, are generally (though not always) associated with increased levels of sICAM-1 and sVCAM-1. 26,[37][38][39][40][41][42][43] It is unclear whether the observed elevations are because of direct effects or to subclinical atherosclerosis. Certainly, elevated levels of both sICAM-1 and sVCAM-1 have been documented in patients with essential hypertension without overt atherosclerotic disease, 39 although in this cohort of elderly (mean age 69 years) hypertensive men it seems likely that some would have inapparent disease.…”

“…26,[37][38][39][40][41][42][43] It is unclear whether the observed elevations are because of direct effects or to subclinical atherosclerosis. Certainly, elevated levels of both sICAM-1 and sVCAM-1 have been documented in patients with essential hypertension without overt atherosclerotic disease, 39 although in this cohort of elderly (mean age 69 years) hypertensive men it seems likely that some would have inapparent disease. The data from Rizzoni et al, 26 showing significant elevations sICAM-1 and sVCAM-1 in patients with hypertension and normal intima-media thickness, do, however, suggest that hypertension may play a direct role.…”