The state of renin-aldosterone system in patients with resistant arterial hypertension

Purpose. The understanding of pathophysiology and clinical characteristics of resistant hypertension (RH) remains elusive. The aim of this work was to study the relationships between clinical course of RH and levels of renin and aldosterone (AS). Materials and methods. A total of 47 patients with...

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Bibliographic Details
Main Author: О. H. Оbertynska
Format: Article
Language:English
Published: Zaporizhzhia State Medical and Pharmaceutical University 2019-06-01
Series:Zaporožskij Medicinskij Žurnal
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Online Access:http://zmj.zsmu.edu.ua/article/view/168951/169277
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Summary:Purpose. The understanding of pathophysiology and clinical characteristics of resistant hypertension (RH) remains elusive. The aim of this work was to study the relationships between clinical course of RH and levels of renin and aldosterone (AS). Materials and methods. A total of 47 patients with true RH were included in the study. The control group included 50 patients with controlled arterial hypertension (CAH). All patients underwent general clinical examination, calculation of body mass index (BMI), office blood pressure measurement, determination of plasma potassium, AS and active renin concentrations (ARC), assessment of plasma aldosterone-to-renin ratio, urinary albumin excretion, albumin-creatinine ratio (ACR), uric acid, serum creatinine, calculation of glomerular filtration rate (GFR) by Cockcroft–Gault formula, echocardiography. Results. AS and ARC levels were significantly higher (AS 145.21 ± 11.90 ng/ml and 122.04 ± 8.60 ng/ml, P < 0.001; ARC 18.21 ± 3.50 ng/ml and 14.40 ± 2.20 ng/ml, P < 0.05) in patients with RH compared to those with CAH, respectively. At the same time, among patients with RH, only 38 % had a normal ARC; increased ARC was in 27 % and reduced ARC was in 35 % of patients. Among patients with CAH, 78 % had a normal ARC; increased ARC was in 7 % and reduced ARC was in 15 % of patients. In patients with CAH, there was negative correlation between AS and ARC levels (r = -0.38, P < 0.05), at the same time in patients with RH, no correlation was found between AS and ARC levels. However, in patients with RH, there were negative correlations between AS, ARC and GFR (r = -0.36, P < 0.05; r = -0.32, P < 0.05, respectively); positive – ARC and left ventricular mass index (r = 0.43, P < 0.05); AS and ACR (r = 0.76, Р < 0.01); AS and left ventricular end-diastolic volume (r = 0.38, P < 0.05). Moreover, significant correlations were found between ARC and BMI (r = 0.59, P < 0.001), AS and BMI (r = 0.42, P < 0.05). Conclusions. The results indicate that in patients with RH, higher renin and AS levels are mediated by overweight as well as renin and AS have a different influence on target organs in RH. Furthermore, stimulation of AS production occurs regardless of the renin-angiotensin system and angiotensin II effects. The group of patients with RH is not homogeneous according to renin concentration and “low-renin” and “high-renin” hypertension are more frequently registered among them. It seems that pathophysiologic mechanisms are different in each case and need to be identified for the selection of antihypertensive agents to treat patients successfully.
ISSN:2306-4145
2310-1210