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Introduction The aim of this study was to assess the relations between plasma renin activity (PRA), serum aldosterone concentration (ALDO) and selected asymptomatic organ damage (AOD) indices in mild primary arterial hypertension (AH). Material and methods We measured PRA, ALDO, and selected AOD indices (carotid-femoral pulse wave velocity (cfPWV), central aortic pulse pressure (cPP), estimated glomerular filtration rate (eGFR)) in 122 patients with untreated AH. Results Patients with high PRA (≥ 0.65 ng/ml/h) were characterized by lower plasma sodium and aldosterone to renin ratio (ARR), higher ALDO, but a similar level of AOD indices compared to patients with low PRA. cfPWV ( p = 0.04) and cPP ( p = 0.019) increased with ARR, while eGFR decreased with ALDO ( p = 0.008). Only eGFR was independently correlated with ALDO. In subjects with simultaneously high PRA and ARR values, we found significantly higher cfPWV ( p = 0.02) and cPP ( p = 0.04) and lower eGFR ( p = 0.02) than in those with high PRA but low ARR values. Conclusions Assessment of the influence of the renin-angiotensin-aldosterone system (RAAS) on AOD should include the relationship between renin and aldosterone. The PRA itself has no predictive value for AOD. More advanced arterial stiffness and renal impairment are associated with increased PRA and ARR. The RAAS activity might be useful in AOD prediction and hypertension severity assessment.

Introduction:The aim of the study was to evaluate clinical and biochemical differences between patients with low-renin and high-renin primary arterial hypertension (AH), mainly in reference to serum lipids, and to identify factors determining lipid concentrations.Materials and methods:In untreated patients with AH stage 1 we measured plasma renin activity (PRA) and subdivided the group into low-renin (PRA < 0.65 ng/mL/h) and high-renin (PRA ⩾ 0.65 ng/mL/h) AH. We compared office and 24-h ambulatory blood pressure, serum aldosterone, lipids and selected biochemical parameters between subgroups. Factors determining lipid concentration in both subgroups were assessed in regression analysis.Results:Patients with high-renin hypertension (N = 58) were characterized by higher heart rate (p = 0.04), lower serum sodium (p < 0.01) and aldosterone-to-renin ratio (p < 0.01), and significantly higher serum aldosterone (p = 0.03), albumin (p < 0.01), total protein (p < 0.01), total cholesterol (p = 0.01) and low-density lipoprotein cholesterol (LDL-C) (p = 0.04) than low-renin subjects (N = 39). In univariate linear regression, only PRA in the low-renin group was in a positive relationship with LDL-C (R2 = 0.15, β = 1.53 and p = 0.013); this association remained significant after adjustment for age, sex, and serum albumin and aldosterone concentrations.Conclusions:Higher serum levels of total and LDL-C characterized high-renin subjects, but the association between LDL-C level and PRA existed only in low-renin primary AH.

Background: Atherosclerosis is as a systemic inflammatory disease associated with the activation of many mediators, including matrix metalloproteinases (MMPs), and may be amplified by abnormal high serum uric acid (UA) concentration (hyperuricemia, HU). The aim of the study was to determine the relationship between serum UA concentration and activity of MMPs and their correlation with the hypertension-mediated organ damage (HMOD) intensity. Methods: One hundred and nine patients untreated with antihypertensive, hypolipemic or uratelowering drugs with diagnosed stage 1-2 essential hypertension were included in this study. In all participants blood pressure (BP) was measured, carotid-femoral pulse wave velocity (PWV), intima-media thickness (IMT), echocardiography and blood tests including UA, lipids and serum concentrations of MMPs (1, 2, 3, 9) were observed. The participants were divided into hyper-and normuricemic groups. Results: Uric acid concentration in the whole study group positively correlated with some HMOD parameters (IMT, PWV, left ventricular mass index, left atrial dimension). Among the studied metalloproteinases only MMP-3 activity positively correlated with serum UA concentration independently of age, body mass index and serum lipids (R2 = 0.11, p = 0.048). Multivariate regression analysis showed positive association between IMT and BP, UA concentration and MMP-3 activity, independently of waist circumference and serum lipids (R2 = 0.328, p < 0.002). Patients with HU were characterized by higher activity of MMP-3 than those without (19.41 [14.45; 21.74] vs. 13.98 [9.52; 18.97] ng/mL, p = 0.016). Conclusions: The present results may support the thesis that UA and the increased by UA activity of MMPs may take part in the development of HMOD, especially IMT.

Left atrial enlargement (LAE) is a risk factor for cardiovascular complications and death. In hypertensive patients, LAE is usually due to left ventricular (LV) hypertrophy and diastolic dysfunction. We aimed to identify factors associated with LAE in patients with increased and normal left ventricular mass index (LVMI) with reference to pulsatile and steady components of blood pressure (BP).The study was carried out as a cross-sectional observation. In a group of inhabitants of suburban area of Cracow, Poland, we measured office, ambulatory and central BP, carotid-femoral pulse wave velocity (PWV), as well as echocardiographic indices and gathered anthropometric data, information on habits and relevant medical history. Further, with division according to sex-stratified dichotomised LVMI, we performed correlation analysis to identify possibly significant relations between measures of left atrial volume and other studied parameters. We also fitted regression models in order to assess the respective value of steady and pulsatile BP components as factors related to measures of left atrial volume.The mean age of 205 patients (136 females-66%) was 53.6 ± 8.3 years. We found higher values of PWV, office, ambulatory and central BPs in the group of LVMI above median value. This group had also greater left atrial volume index (LAVI), which correlated with LVMI (r = 0.36, P < .001) and ratio of early diastolic mitral peak flow velocity to early diastolic mitral annulus mean velocity in tissue Doppler imaging (E/e') (r = 0.24, P = .04).In the group of LVMI below the median, LAVI correlated with pulsatile and steady BP components. LAVI was independently predicted by mean arterial pressure (MAP) obtained from both ambulatory (MAP24h, β= 0.15; P = .045) and office measurements (MAPoffice, β = 0.35; P = .004), but not by pulse pressure.LV mass and function are the main determinants of LAVI. However, in persons with lower LV mass, LAVI depends on the steady component of blood pressure, but not pulsatile one. Increased LAVI reflects early changes in response to systemic blood pressure elevation.