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P-680: Endothelial and platelet activation in severe, uncontrolled hypertension: Absolute effect of extreme blood pressure elevation on soluble adhesion molecules and CD62 (P-selectin)

Introduction: Although patients with extreme elevations of blood pressure (BP) are at especially high risk for acute target organ injury, the molecular mechanisms by which severe uncontrolled hypertension (HT) is translated into acute target organ injury are not established. Whether adhesion molecul...

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Published in:American journal of hypertension 2001-04, Vol.14 (S1), p.257A-257A
Main Authors: Preston, Richard A., Ledford, Marlies, Materson, Barry J., Lai, Shenghan, Baltodano, Neyton M., Alonso, Alberto
Format: Article
Language:English
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Summary:Introduction: Although patients with extreme elevations of blood pressure (BP) are at especially high risk for acute target organ injury, the molecular mechanisms by which severe uncontrolled hypertension (HT) is translated into acute target organ injury are not established. Whether adhesion molecules and CD62 (P-selectin) are mediators of acute target organ injury in patients with severe uncontrolled hypertension is not known. The aim of our study is to ascertain the effect of extreme elevation of BP on endothelial and platelet injury/activation as measured by expression of soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1) and CD62. Methods: Comparison of sVCAM-1, sICAM-1, and CD62 among 3 groups: Untreated severe hypertensives (Severe HT; n=24) with diastolic blood pressure (DBP)≥120 mm Hg, mild hypertensives (Mild HT; n=19) with DBP≤100 mm Hg, and normotensive control subjects (NT; n=15). Results [Expressed as mean (SD)]: sVCAM-1 (p=.0001), sICAM-1 (p=.006), and CD62(p=.0006) were greater in Severe HT and Mild HT than NT but did not differ between Severe HT and Mild HT. By regression analysis, there appeared to be no relationship between the absolute level of BP and the concentrations of sVCAM-1 and sICAM-1. CD62 showed a significant but weak relationship with systolic (p=.001, R squared=.19), diastolic (p=.006, R squared=.14), and pulse pressure (p=.003, R squared= .16). Conclusion: Our results suggest that concentrations of soluble adhesion molecules and CD62 may depend more strongly upon factors in the hypertensive microenvironment other than the absolute level of BP. There does not seem to be a dose-response between these markers and BP per se. Even mild elevation of BP may be sufficient to activate the expression of adhesion molecules and CD62. Other mechanisms than endothelial cell and platelet activation/injury may be important in producing target organ injury in severe uncontrolled hypertension. (See Table) Severe HT Mild HT Normotensive SBP (mm Hg) 195 (26) 145 (10) 121 (9) DBP (mm Hg) 127 (7) 96 (1) 79 (6) Pulse Pressure 68 (23) 46 (10) 42 (7) sVCAM-1 (ng/ml) 635 (237) 690 (215) 389 (72) sICAM-1 (ng/ml) 234 (88) 262 (74) 179 (45) CD62 (Mabs/plt) 977 (371) 978 (234) 604 (194)
ISSN:0895-7061
1941-7225
1879-1905
DOI:10.1016/S0895-7061(01)02010-6