Vol 24, No 1 (2020)
Original paper
Published online: 2020-03-10

open access

Page views 656
Article views/downloads 687
Get Citation

Connect on Social Media

Connect on Social Media

Blood pressure and its circadian pattern in obese and lean premenopausal women

José Silva-Nunes123, Miguel Brito1, Luisa Veiga1
Arterial Hypertension 2020;24(1):30-37.

Abstract

Background. Obesity is frequently referred to as an independent risk factor for high blood pressure and hypertension is very prevalent among obese people. The aims of this study were: to compare office-based and 24 h blood pressure (BP) and its circadian pattern between lean and obese women; to study correlations between BP, insulin resistance (IR) and markers of subclinical inflammation/early atherosclerosis.

Material and methods. Eighty-eight lean and 107 otherwise healthy obese women were characterized for anthropometrics, BP (office-based determinations and 24 h ABPM) and for glucose, insulin, triglycerides, inteleukin 6 (IL-6), tumor necrosis factor alpha (TNF-a), high-sensitivity C reactive protein (hs-CRP), retinol-binding protein 4 (RBP-4), leptin, adiponectin, resistin, monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1 (ICAM-1), and vascular-cellular adhesion molecule 1 (VCAM-1). Insulin resistance was determined by homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and McAuley indexes (also Matsuda in obese).

Results. Obese group presented higher office-based systolic/diastolic BP, systolic ambulatory blood pressure monitoring (ABPM), and more non-dippers. HOMA-IR and body fat was correlated to systolic (r2 = 0.176) and glucose to diastolic (p = 0.008; r = 0.256) ABPM. Age, QUICKI, and TNF-a was correlated with dipping (r2 = 0.172); adiponectin, age, BMI, and glucose to systolic (r2 = 0.226) and diastolic (r2 = 0.215) office-based BP. Concerning lean women, MCP-1 was associated with diastolic ABPM (p = 0.013; r = 0.267). Systolic office-based BP was associated with waist-to-hip ratio (p = 0.01; r = 0.273); this and RBP-4 was correlated with office-based diastolic BP (r2 = 0.12).

Conclusion. Although relatively healthy, obese women present higher BP than lean. Anthropometrics, IR, and fasting glucose all influence BP in obesity; additionally, IR is involved in non-dipping. No strong correlation exists between BP/dipping and subclinical inflammation in either group of women. 

Article available in PDF format

View PDF Download PDF file

References

  1. Kotchen TA. Obesity-related hypertension: epidemiology, pathophysiology, and clinical management. Am J Hypertens. 2010; 23(11): 1170–1178.
  2. Nguyen NT, Magno CP, Lane KT, et al. Association of hypertension, diabetes, dyslipidemia, and metabolic syndrome with obesity: findings from the National Health and Nutrition Examination Survey, 1999 to 2004. J Am Coll Surg. 2008; 207(6): 928–934.
  3. Narkiewicz K. Diagnosis and management of hypertension in obesity. Obes Rev. 2006; 7(2): 155–162.
  4. Zhou J, Qin G. Adipocyte dysfunction and hypertension. Am J Cardiovasc Dis. 2012; 2(2): 143–149.
  5. Dorresteijn JAN, Visseren FLJ, Spiering W. Mechanisms linking obesity to hypertension. Obes Rev. 2012; 13(1): 17–26.
  6. Hajer GR, van Haeften TW, Visseren FLJ. Adipose tissue dysfunction in obesity, diabetes, and vascular diseases. Eur Heart J. 2008; 29(24): 2959–2971.
  7. Seravalle G, Grassi G. Obesity and hypertension. Pharmaco Res. 2017; 122: 1–7.
  8. Wang ZV, Scherer PE. Adiponectin, cardiovascular function, and hypertension. Hypertension. 2008; 51(1): 8–14.
  9. Orlando A, Nava E, Giussani M, et al. Adiponectin and Cardiovascular Risk. From Pathophysiology to Clinic: Focus on Children and Adolescents. Int J Mol Sci. 2019; 20(13).
  10. Li FYL, Cheng KKY, Lam KSL, et al. Cross-talk between adipose tissue and vasculature: role of adiponectin. Acta Physiol (Oxf). 2011; 203(1): 167–180.
  11. Kalil GZ, Haynes WG. Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications. Hypertens Res. 2012; 35(1): 4–16.
  12. Lambert EA, Esler MD, Schlaich MP, et al. Obesity-Associated Organ Damage and Sympathetic Nervous Activity. Hypertension. 2019; 73(6): 1150–1159.
  13. Dauphinot V, Gosse P, Kossovsky MP, et al. Autonomic nervous system activity is independently associated with the risk of shift in the non-dipper blood pressure pattern. Hypertens Res. 2010; 33(10): 1032–1037.
  14. Mancia G, De Ba, Dominiczak A, et al. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens. 2007; 25(6): 1105–1187.
  15. Japanese Circulation Society Joint Working Group. Guidelines for the clinical use of 24 hour ambulatory blood pressure monitoring (ABPM) (JCS 2010). Circ J. 2012; 76(2): 508–19.
  16. Franklin SS, Gustin W, Wong ND, et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation. 1997; 96(1): 308–315.
  17. Sowers JR, Epstein M, Frohlich ED, et al. Diabetes mellitus and associated hypertension, vascular disease, and nephropathy. An update. Hypertension. 1995; 26(6 Pt 1): 869–879.
  18. Gress TW, Nieto FJ, Shahar E, et al. Hypertension and antihypertensive therapy as risk factors for type 2 diabetes mellitus. Atherosclerosis Risk in Communities Study. N Engl J Med. 2000; 342(13): 905–912.
  19. Schmieder RE, Tschöpe D, Koch C, et al. DIALOGUE study group.. Individualised treatment targets in patients with type-2 diabetes and hypertension. Cardiovasc Diabetol. 2018; 17(1): 18.
  20. Kurukulasuriya LR, Stas S, Lastra G, et al. Hypertension in obesity. Med Clin North Am. 2011; 95(5): 903–917.
  21. Kotsis V, Stabouli S, Bouldin M, et al. Impact of obesity on 24-hour ambulatory blood pressure and hypertension. Hypertension. 2005; 45(4): 602–607.
  22. Fantuzzi G, Mazzone T. Adipose tissue and atherosclerosis: exploring the connection. Arterioscler Thromb Vasc Biol. 2007; 27(5): 996–1003.
  23. Antuna-Puente B, Feve B, Fellahi S, et al. Adipokines: the missing link between insulin resistance and obesity. Diabetes Metab. 2008; 34(1): 2–11.
  24. Ramseyer VD, Hong NJ, Garvin JL. Tumor necrosis factor α decreases nitric oxide synthase type 3 expression primarily via Rho/Rho kinase in the thick ascending limb. Hypertension. 2012; 59(6): 1145–1150.
  25. Engin A. Endothelial Dysfunction in Obesity. Adv Exp Med Biol. 2017; 960: 345–379.
  26. Hering D, Somers VK, Kara T, et al. Sympathetic neural responses to smoking are age dependent. J Hypertens. 2006; 24(4): 691–695.
  27. Primeau V, Coderre L, Karelis AD, et al. Characterizing the profile of obese patients who are metabolically healthy. Int J Obes (Lond). 2011; 35(7): 971–981.
  28. Beh S. Is metabolically healthy obesity a useful concept? Diabet Med. 2019; 36(5): 539–545.