Cold Pressor Test Raises Serum Concentrations of ICAM-1, VCAM-1, and E-Selectin in Normotensive and Hypertensive Patients

Abstract

In patients with essential hypertension, elevated soluble E-selectin (sE-selectin) levels may indicate endothelial cell injury or activation. We therefore sought to ascertain whether arterial blood pressure increased by the cold pressor test can modify serum concentrations of sE-selectin and other soluble forms of adhesion molecules, such as soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), or the expression of any adhesion molecules in circulating monocytes and lymphocytes. Our findings show that levels of sE-selectin, sVCAM-1, and sICAM-1 are higher in patients with essential hypertension than in normotensive subjects (sICAM-1, 380±52 versus 262±96 ng/mL, P <.05; sVCAM-1, 720±52 versus 625±38 ng/mL, P <.05; and sE-selectin, 75±21 versus 61±22 ng/mL, P <.05). Furthermore, in normotensive and hypertensive patients, the cold pressor test caused an increase in serum concentrations of sICAM-1, sVCAM-1, and sE-selectin, but it did not cause changes in the expression of adhesion molecules in circulating monocytes and lymphocytes. High arterial blood pressure may therefore increase the production of serum adhesion molecules, probably through endothelial activation.

Effects of efonidipine on platelet and monocyte activation markers in hypertensive patients with and without type 2 diabetes mellitus

“…These adhesion molecules include E-selectin, which is produced by endothelial cells, and P-selectin, which is a product of both endothelial cells and platelets, 51 and a relation to adhesive molecules has previously been reported in some hypertensive patients. [52][53][54][55] In the present study, we found that Eselectin levels were significantly increased in the hypertension patients with diabetes. An increase in activated platelets and PDMPs, leading to monocyte infiltration of the arterial wall, has been suggested to be important in the development of atheroscler-osis.…”

Effect of the HMG-CoA Reductase Inhibitors on Blood Pressure in Patients With Essential Hypertension and Primary Hypercholesterolemia

“…4 -7 This interpretation is supported by the favorable effect of pravastatin on the cold pressor test and by the reduction in levels of circulating endothelin-1 after pravastatin. Other studies 27,28 have shown that the blood pressure increase caused by the cold pressor test is associated with an increase in circulating cell adhesion molecules and endothelin. In the present study, measures of biological markers of endothelial function other than endothelin-1 were not available.…”

Nitric oxide and cell adhesion molecules in essential hypertension: a case control study

“…The multivariate logistic analysis suggested that individuals with E-selectin levels higher than 44 ng/ml had a five times higher odds to develop hypertension (odds ratio 5.2 (2.21-12.24) at 95% CI, Po0.01). Beumi et al 9 suggested that the alterations in the serum concentrations of E-selectin in hypertensive patients may be a sign of simple endothelial activation to vessels caused by blood pressure increase. Blann et al 10 found a positive correlation between the levels of E-selectin and diastolic blood pressure in essential hypertension and suggested that raised levels of E-selectin in hypertension indicate endothelial activation rather than endothelial cell injury.…”

“…The multivariate logistic analysis suggested that individuals with sVCAM-1 levels higher than 338 ng/ml had a 19 times higher odds to develop hypertension (odds ratio 19.67 (5.51-70.23) at 95% CI, Po0.01). Beumi et al 9 reported a borderline increase in the levels of sVCAM-1 in the patients with essential hypertension and suggested that high arterial blood pressure because of increased vascular distending and transmural pressure might increase the production of sVCAM-1 probably through endothelial activation. However, Beumi et al 9 did not find any correlation between the levels of sVCAM-1 and systolic and diastolic blood pressure.…”

“…Beumi et al 9 reported a borderline increase in the levels of sVCAM-1 in the patients with essential hypertension and suggested that high arterial blood pressure because of increased vascular distending and transmural pressure might increase the production of sVCAM-1 probably through endothelial activation. However, Beumi et al 9 did not find any correlation between the levels of sVCAM-1 and systolic and diastolic blood pressure. Similarly, we did not find any correlation between the systolic/diastolic blood pressure and sVCAM-1 levels.…”