The relationship between plasma renin activity and serum lipid profiles in patients with primary arterial hypertension

Abstract

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.

Features of hemodynamic and metabolic disorders in obese patients with resistant hypertension

“…The literature suggests that between 50% and 80% of patients with AH who are prescribed antihypertensive drugs show suboptimal adherence to treatment. In many cases, this high percentage of failure to reach target BP levels is at least in part due to the large number of drugs, the complexity of their dosage, the high incidence of adverse reactions, poor patientphysician relationships, and the inertia of the clinician with reduced adherence to treatment [2,10].…”

Renin–Angiotensin System in Liver Metabolism: Gender Differences and Role of Incretins

“…The GLP-1 receptor agonist acts neuroprotectively that minimizes the harmful effects of maternal food restriction [ 58 ]. AngII has been shown to modulate lipolysis, lipogenesis and adipocyte differentiation [ 38 ]. AngII also, via AngII receptor type 1 (AT1), stimulates cholesterol synthesis, low-density lipoprotein cholesterol (LDL-C) oxidation and its incorporation into the vascular wall [ 38 ].…”

“…Chronic blockade of AT1 protects the liver from triacylglycerol (TAG) accumulation, particularly during a glucose load [ 40 ]. Some clinical studies indicate that a reduction in hyperlipidemia and RAS blockade may have a synergistic effect [ 38 ]. RAS inhibitors that are used as classical antihypertensive drugs can lessen the occurrence of T2DM [ 6 ] and improve NAFLD and liver injury [ 3 ].…”

“…RAS overactivity represented by the increase in local AngII and activation of AT1R may lead to liver dysfunction promoting inflammation, liver steatosis and lipid metabolism dysregulation [ 38 ]. In metabolic disease of the liver it has been shown there is an imbalance between ACE/AngII/AT1 and ACE2/Ang(1-7)/Mas [ 31 ].…”

Features of the Activity of Separate Components of the Renin-Angiotensin-Aldosterone System in Arterial Hypertension and Concomitant Obesity

“…Цей фенотип був відмінним від первинного альдостеронізму і називався НРАГ, а наступні дослідження описували його як стан, більш поширений у осіб африканського походження та літніх людей, які також схильні до натрій-залежної гіпертензії [6]. У наступні десятиліття було припущення, що НРАГ може представляти собою гетерогенну суміш етіологій, і може включати стани надмірної активації мінералокортикоїдних рецепторів (оскільки спочатку у осіб з НРАГ виявлялося помітне зниження АТ у відповідь на дію антагоніста мінералокортикоїдних рецепторів (спіронолактона) та інгібітора синтезу стероїдів надниркових залоз (аміноглютетеміда)) [7][8][9][10][11].…”