open access

Vol 26, No 3 (2022)
Original paper
Published online: 2022-05-06
Get Citation

Association of soluble E-selectin and morning blood pressure surge in patients with essential hypertension

Mohamed Yahia Abd Alkhalik1, Mahmoud Ezz Elarab1, Eman Masoud Abd El Gayed2
DOI: 10.5603/AH.a2022.0008
·
Arterial Hypertension 2022;26(3):122-128.
Affiliations
  1. Department of Cardiology, Faculty of medicine, Menoufia University, Shebin Elkom, Egypt
  2. Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Menoufia University, Shebin Elkom, Egypt

open access

Vol 26, No 3 (2022)
ORIGINAL PAPERS
Published online: 2022-05-06

Abstract

Background: Elevated soluble E-selectin which reflects a state of endothelial activation with subsequent vasoconstriction may elevate morning blood pressure (BP) surge. This study aimed to analyze soluble E-selectin serum concentrations in patients with essential hypertension against normotensive healthy individuals and to find a role of such molecule in the phenomenon of morning BP surge.

Material and methods: In this case-control study, a 24-hour ambulatory blood pressure monitoring with recording of morning BP surge and serum soluble E-selectin levels were measured for a total of 90 patients (60 patients with essential hypertension and 30 normotensive subjects as a control).

Results: Hypertensive patients had higher body mass index in comparison to control subjects (30.7 ± 2.3 kg/m2 vs. 27 ± 3.2 kg/m2, p < 0.001). Serum uric acid levels were higher in hypertensive patients than control subjects (7.26 ± 2.60 mg/dL vs. 5.92 ± 1.15 mg/dL, p = 0.028). Hypertensive patients had higher left ventricular mass index (LVMI) (110.5 ± 19.2 g/m2 vs. 99.8 ± 9.5 g/m2, p = 0.001). Patients with essential hypertension have higher level of soluble E-selectin than normotensive participants (180.6 ± 96.1 vs. 75.9 ± 31.5 ng/mL, p < 0.001). Soluble E-selectin was positively correlated with morning BP surge (r = 0.696, p ≤ 0.001).

Conclusion: Patients with essential hypertension have higher level of soluble E-selectin than normotensive. Soluble E-selectin was positively correlated with morning BP surge.

Abstract

Background: Elevated soluble E-selectin which reflects a state of endothelial activation with subsequent vasoconstriction may elevate morning blood pressure (BP) surge. This study aimed to analyze soluble E-selectin serum concentrations in patients with essential hypertension against normotensive healthy individuals and to find a role of such molecule in the phenomenon of morning BP surge.

Material and methods: In this case-control study, a 24-hour ambulatory blood pressure monitoring with recording of morning BP surge and serum soluble E-selectin levels were measured for a total of 90 patients (60 patients with essential hypertension and 30 normotensive subjects as a control).

Results: Hypertensive patients had higher body mass index in comparison to control subjects (30.7 ± 2.3 kg/m2 vs. 27 ± 3.2 kg/m2, p < 0.001). Serum uric acid levels were higher in hypertensive patients than control subjects (7.26 ± 2.60 mg/dL vs. 5.92 ± 1.15 mg/dL, p = 0.028). Hypertensive patients had higher left ventricular mass index (LVMI) (110.5 ± 19.2 g/m2 vs. 99.8 ± 9.5 g/m2, p = 0.001). Patients with essential hypertension have higher level of soluble E-selectin than normotensive participants (180.6 ± 96.1 vs. 75.9 ± 31.5 ng/mL, p < 0.001). Soluble E-selectin was positively correlated with morning BP surge (r = 0.696, p ≤ 0.001).

Conclusion: Patients with essential hypertension have higher level of soluble E-selectin than normotensive. Soluble E-selectin was positively correlated with morning BP surge.

Get Citation

Keywords

hypertension; soluble E-selectin; morning blood pressure surge

About this article
Title

Association of soluble E-selectin and morning blood pressure surge in patients with essential hypertension

Journal

Arterial Hypertension

Issue

Vol 26, No 3 (2022)

Article type

Original paper

Pages

122-128

Published online

2022-05-06

Page views

823

Article views/downloads

53

DOI

10.5603/AH.a2022.0008

Bibliographic record

Arterial Hypertension 2022;26(3):122-128.

Keywords

hypertension
soluble E-selectin
morning blood pressure surge

Authors

Mohamed Yahia Abd Alkhalik
Mahmoud Ezz Elarab
Eman Masoud Abd El Gayed

References (32)
  1. Neutel JM, Schumacher H, Gosse P, et al. Magnitude of the early morning blood pressure surge in untreated hypertensive patients: a pooled analysis. Int J Clin Pract. 2008; 62(11): 1654–1663.
  2. Kaplan NM. Morning surge in blood pressure. Circulation. 2003; 107(10): 1347.
  3. Luo Yu, Wang Yl, Wu Yb, et al. Association between the rate of the morning surge in blood pressure and cardiovascular events and stroke. Chin Med J (Engl). 2013; 126(3): 510–514.
  4. Kario K, Yano Y, Matsuo T, et al. Additional impact of morning haemostatic risk factors and morning blood pressure surge on stroke risk in older Japanese hypertensive patients. Eur Heart J. 2011; 32(5): 574–580.
  5. Moore KJ, Tabas I. Macrophages in the pathogenesis of atherosclerosis. Cell. 2011; 145(3): 341–355.
  6. Kuroda YT, Komamura K, Tatsumi R, et al. Vascular cell adhesion molecule-1 as a biochemical marker of left ventricular mass in the patients with hypertension. Am J Hypertens. 2001; 14(9 Pt 1): 868–872.
  7. Ferri C, Desideri G, Valenti M, et al. Early upregulation of endothelial adhesion molecules in obese hypertensive men. Hypertension. 1999; 34(4 Pt 1): 568–573.
  8. Williams B, Mancia G, Spiering W, et al. ESC Scientific Document Group. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J. 2018; 39(33): 3021–3104.
  9. Price DT, Loscalzo J. Cellular adhesion molecules and atherogenesis. Am J Med. 1999; 107(1): 85–97.
  10. Malmqvist K, Wallén HN, Held C, et al. Soluble cell adhesion molecules in hypertensive concentric left ventricular hypertrophy. J Hypertens. 2002; 20(8): 1563–1569.
  11. Nomura S, Kanazawa S, Fukuhara S. Effects of efonidipine on platelet and monocyte activation markers in hypertensive patients with and without type 2 diabetes mellitus. J Hum Hypertens. 2002; 16(8): 539–547.
  12. Miller M, Kerry S, Cook D, et al. Cellular adhesion molecules and blood pressure. J Hypertens. 2004; 22(4): 705–711.
  13. Palomo I, Marín P, Alarcón M, et al. Patients with essential hypertension present higher levels of sE-selectin and sVCAM-1 than normotensive volunteers. Clin Exp Hypertens. 2003; 25(8): 517–523.
  14. DeSouza CA, Dengel DR, Macko RF, et al. Elevated levels of circulating cell adhesion molecules in uncomplicated essential hypertension. Am J Hypertens. 1997; 10(12 Pt 1): 1335–1341.
  15. Jilma B, Li-Saw-Hee FL, Wagner OF, et al. Effect of antihypertensive therapy using enalapril or losartan on haemostatic markers in essential hypertension: a pilot prospective randomised double-blind parallel group trial. Int J Cardiol. 2001; 78(3): 241–246.
  16. Hlubocká Z, Umnerová V, Heller S, et al. Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors. J Hum Hypertens. 2002; 16(8): 557–562.
  17. Otto ME, Svatikova A, Barretto RB, et al. Early morning attenuation of endothelial function in healthy humans. Circulation. 2004; 109(21): 2507–2510.
  18. Solini A, Stea F, Santini E, et al. Adipocytokine levels mark endothelial function in normotensive individuals. Cardiovasc Diabetol. 2012; 11: 103.
  19. Knudsen ST, Jeppesen P, Frederiksen CA, et al. Endothelial dysfunction, ambulatory pulse pressure and albuminuria are associated in Type 2 diabetic subjects. Diabet Med. 2007; 24(8): 911–915.
  20. Ceravolo R, Maio R, Pujia A, et al. Pulse pressure and endothelial dysfunction in never-treated hypertensive patients. J Am Coll Cardiol. 2003; 41(10): 1753–1758.
  21. Amar J, Ruidavets JB, Bal Dit Sollier C, et al. Relationship between C reactive protein and pulse pressure is not mediated by atherosclerosis or aortic stiffness. J Hypertens. 2004; 22(2): 349–355.
  22. Blake GJ, Rifai N, Buring JE, et al. Blood pressure, C-reactive protein, and risk of future cardiovascular events. Circulation. 2003; 108(24): 2993–2999.
  23. van Bussel BC, Schouten F, Henry RM, et al. Endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness over a 6-year period. Hypertension. 2011; 58(4): 588–595.
  24. de Faria AP, Ritter AM, Sabbatini AR, et al. Deregulation of Soluble Adhesion Molecules in Resistant Hypertension and Its Role in Cardiovascular Remodeling. Circ J. 2016; 80(5): 1196–1201.
  25. Turak O, Afsar B, Ozcan F, et al. Relationship between elevated morning blood pressure surge, uric acid, and cardiovascular outcomes in hypertensive patients. J Clin Hypertens (Greenwich). 2014; 16(7): 530–535.
  26. Yu MA, Sánchez-Lozada LG, Johnson RJ, et al. Oxidative stress with an activation of the renin-angiotensin system in human vascular endothelial cells as a novel mechanism of uric acid-induced endothelial dysfunction. J Hypertens. 2010; 28(6): 1234–1242.
  27. Soletsky B, Feig DI. Uric acid reduction rectifies prehypertension in obese adolescents. Hypertension. 2012; 60(5): 1148–1156.
  28. Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial. JAMA. 2008; 300(8): 924–932.
  29. Lanaspa MA, Andres-Hernando A, Kuwabara M. Uric acid and hypertension. Hypertens Res. 2020; 43(8): 832–834.
  30. Hossain FB, Adhikary G, Chowdhury AB, et al. Association between body mass index (BMI) and hypertension in south Asian population: evidence from nationally-representative surveys. Clin Hypertens. 2019; 25: 28.
  31. Carey RM, Muntner P, Bosworth HB, et al. Prevention and Control of Hypertension: JACC Health Promotion Series. J Am Coll Cardiol. 2018; 72(11): 1278–1293.
  32. Olszanecka-Glinianowicz M, Dudek D, Filipiak K, et al. Treatment of overweight and obesity during and after a pandemic. Let’s not wait for the development of complications — new guidelines for doctors. Arterial Hypertension. 2020; 24(3): 93–105.

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail: viamedica@viamedica.pl