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Primary aldosteronism (PA) is the most common reason of secondary hypertension, that can be cured surgically or treated with targeting medical treatment. In many cases PA is not diagnosed on time, leading to aldosterone-specific cardiovascular and nephritic lesions. Effective methods of treatment make it reasonable to perform case detection testing for PA at least once in all patients with hypertension. Mayo Clinic approach is aimed to simplify primary case detection testing. There is no need to use plasma aldosterone concentration/plasma renin activity ratio, all tests can be completed, whilst the patient is taking antihypertensive and other medications. The next step is confirmatory testing. The choice of pharmacological or surgical therapy depends on the results of computed tomography scans of the adrenal glands and adrenal venous sampling. The last one is performed only after discussing with patient the advantages and disadvantages of all therapy methods and positive intention to surgery. Laparoscopic unilateral adrenalectomy is the procedure of choice in patients with unilateral adrenal disease. In patients with bilateral aldosterone hypersecretion, the optimal is a low-sodium diet and lifelong treatment with a mineralocorticoid receptor antagonist administered at a dosage to reach a high-normal serum potassium concentration.Первичный гиперальдостеронизм (ПГА) наиболее распространенная причина вторичной артериальной гипертензии, которая поддается либо хирургическому, либо специфическому медикаментозному лечению. В настоящее время ПГА зачастую вовремя не диагностируется, что приводит к необратимому альдостерон-специфическому поражению сердца и почек. Наличие эффективных методов лечения поднимает вопрос о необходимости исключения ПГА у всех пациентов с артериальной гипертензией как минимум однократно. Существующий подход в клинике Мэйо направлен на максимальное упрощение первичной диагностики данного состояния. Отсутствует необходимость расчета альдостерон-ренинового соотношения, в подавляющем большинстве случаев не требуется отмены антигипертензивных и других препаратов. Дальнейший этап диагностики проведение подтверждающего теста. Выбор терапевтической либо хирургической тактики лечения основывается на результатах компьютерной томографии и селективного венозного забора крови. Последний проводится только после обсуждения с пациентом преимуществ и недостатков существующих методов лечения и при положительном настрое на операцию. В случае подтверждения одностороннего поражения в ходе селективного венозного забора крови лапароскопическая односторонняя адреналэктомия является методом выбора и может привести к полному излечению. Пациентам с двусторонним поражением надпочечников показаны низкосолевая диета и пожизненное применение антагонистов минералокортикоидных рецепторов в той дозе, которая позволит достичь высоконормального уровня калия.

Цель. Исследовать основные показатели суточного мониторирования артериального давления (СМАД) и функционального состояния сосудов у женщин с артериальной гипертензией (АГ) в периоде перименопаузы в зависимости от гемодинамического фенотипа, а также их динамику на фоне комплексного лечения с коррекцией статуса витамина D в организме. Материалы и методы. Обследованы 92 женщины с АГ II степени, риск 3, в периоде перименопаузы, представленные равновеликими подгруппами по статусу витамина D: с нормальным уровнем общего 25(OH)D в плазме (1) и его дефицитом/недостаточностью (2). Все пациентки получали унифицированную антигипертензивную терапию, а в подгруппе 2 – дополнительно холекальциферол 2000 МЕ/сут в течение 3 месяцев. Исходно и в конце наблюдения проводилось СМАД с традиционным анализом результатов и с определением гемодинамического фенотипа методом КАСПАД, определялись активность ренина плазмы (АРП), содержание нитратов/нитритов в плазме, эндотелийзависимая вазодилатация (ЭЗВД) и скорость распространения пульсовой волны (СРПВ) реографическим методом. Результаты и обсуждение. Большинство пациенток имели гармонический фенотип (Г) – 60,9%, но преобладали патологические классы (67,4%). На фоне лечения значимо (p, Purpose. To study the main indicators of 24-hour blood pressure (BP) monitoring and the functional state of blood vessels in perimenopausal women with arterial hypertension (AH) depending on the hemodynamic phenotype, as well as their dynamics in complex treatment with vitamin D status correction. Materials and methods. There were examined 92 women with AH of the stage II and risk 3 in the perimenopause period, represented by equal subgroups on vitamin D status: with a normal plasma level of total 25 (OH)D (1) and its deficiency/insufficiency (2). All patients received unified antihypertensive therapy; the subgroup 2 received cholecalciferol 2000 IU/day for 3 months additionally. Initially and at the end of the observation, there were conducted: 24-hour BP monitoring with the traditional analysis of the results and determination of the hemodynamic phenotype with the QARBPP method; determination of plasma renin activity (PRA) and nitrate/nitrite content; endothelium-dependent vasodilation (EDVD) and pulse wave velocity (PWV) with the rheographic method.Results and discussion. Most patients had a harmonic phenotype (H) – 60.9%, but pathological classes prevailed (67.4%). During treatment, the proportion of individuals with normotensive harmonic class H2 increased significantly from 32.6% to 48.9%, independently on the vitamin D status; the average indices of BP and “pressure loads”, especially in women with vitamin D deficiency/insufficiency (p, Кардиология в Беларуси, Выпуск 3 2020

To investigate the plasma concentrations of cytokines and vasoactive molecules in patients with coronary heart disease (CHD) in the presence of hypertension in relation to the angiotensin-converting-enzyme (ACE) inhibitor level reflecting the degree of renin-angiotensin-aldosterone system (RAAS) inhibition.72 patients with NYHA functional class (FC) II-III angina pectoris and 40 healthy persons at the age of 47-65 years were examined in a controlled cohort study. Enzyme immunoassay was employed to determine the serum concentrations of interleukins (IL) (IL-2, IL-12, IL-17A, and IL-24), the vasoactive molecules of bradykinin, serotonin, ACE, angiotensin-II (AT-II), NO, and endothelin-1 (ET-1), and plasma renin activity. In addition, the plasma level of the tetrapeptide N-acetyl-Ser-Asp-Lys-Pro was used as a marker for ACE inhibition.The patients with CHD occurring in the presence of hypertension compared with the apparently healthy individuals displayed decreased ET-1 and NO production along with elevated levels of serotonin, AT-II, as well as IL-17A and IL-12. The found changes were accompanied by reduced renin activity. Thus, the individuals with low ACE inhibitor levels showed more pronounced production of the proinflammatory cytokine IL-17A, as well as high plasma concentrations of ACE and NO. The high ACE inhibitor level that reflects patient adherence to appropriate antihypertensive therapy is associated with the reduced production of IL-2 and with the minimum serum levels of ACE, AT-II, and NO, being characterized by the high production of IL-12 and serotonin at the same time.In patients with CHD and hypertension, the high plasma enzyme inhibitor concentration that reflects the activity of appropriate antihypertensive therapy, by contributing to the strengthening of the mechanisms of relaxation of blood vessels, is associated with the risk for proinflammatory activation of whole blood cells and platelets. The mean ACE inhibitor levels that reflect moderate RAAS suppression and are characterized by a relatively low proinflammatory activation of mononuclear cells may be more preferable than the maximum ones, from the point of view of slowing the progression of the subclinical inflammatory process of the vascular wall and preventing possible CHD exacerbations. This determines the feasibility of estimating the plasma level of an ACE inhibitor to control the depth of inhibition of RAAS activity.Цель исследования. Изучение концентрации в плазме крови больных ишемической болезнью сердца (ИБС), протекающей на фоне артериальной гипертонии (АГ), цитокинов и вазоактивных молекул в зависимости от уровня ингибитора ангиотензинпревращающего фермента (АПФ), отражающего степень угнетения ренин-ангиотензин-альдостероновой системы РААС. Материалы и методы. В ходе контролируемого когортного исследования обследовали 72 пациентов со стенокардией напряжения II-III функционального класса (ФК) по классификации NYHA и 40 здоровых в возрасте 47-65 лет. Методом иммуноферментного анализа в сыворотке крови определяли концентрацию интерлейкинов (ИЛ-2, ИЛ-12, ИЛ-17А, ИЛ-24), вазоактивных молекул брадикинина, серотонина, ангиотензинпревращающего фермента (АПФ), ангиотензина-II (АТ-II), NO, эндотелина-1 (ЭТ-1), а также активность ренина плазмы. Кроме того, в качестве маркера ингибирования АПФ использовали уровень в плазме крови тетрапептида N-ацетил ser-asp-lys-pro. Результаты. У больных ИБС, протекающей на фоне АГ, по сравнению с практически здоровыми лицами наблюдается уменьшение продукции ЭТ-1 и NO, сочетающееся с повышением уровня серотонина, АТ-II, а также ИЛ-17А и ИЛ-12. Выявленные изменения сопровождаются пониженной активностью ренина. При этом у лиц с низким уровнем ингибитора АПФ отмечается более выраженная продукция провоспалительного цитокина ИЛ-17А, а также высокая концентрация в плазме АПФ и NO. Высокий уровень ингибитора АПФ, отражающий приверженность пациентов к соответствующей гипотензивной терапии, ассоциируется с пониженной продукцией ИЛ-2, минимальным уровнем в сыворотке АПФ, АТ-II и NO, характеризуясь в то же время высокой продукцией ИЛ-12 и серотонина. Заключение. У пациентов с ИБС и АГ высокая концентрация ингибитора АПФ в плазме, отражающая активность соответствующей гипотензивной терапии, способствует усилению механизмов расслабления сосудов, ассоциируется с риском провоспалительной активации клеток цельной крови и тромбоцитов. При этом средние уровни ингибитора АПФ, отражающие умеренную степень подавления РААС, характеризующиеся сравнительно низкой провоспалительной активацией мононуклеарных клеток, могут быть более предпочтительны, чем максимальные, с точки зрения замедления прогрессирования субклинического воспалительного процесса в сосудистой стенке и предупреждения возможных обострений ИБС. Это определяет целесообразность определения содержания ингибитора АПФ в плазме для контроля глубины угнетения активности РААС.

Aldosterone levels increase in clinical practice may be due to primary or secondary hyperaldosteronism. Secondary hyperaldosteronism (CAA) is a clinical syndrome caused by increased synthesis of renin juxtaglomerular apparatus of the kidneys in response to lower perfusion pressure in the afferent glomerular arteriole. This mechanism leads to activation of the renin-angiotensin-aldosterone system with a consequent increase in systemic blood pressure. Clinically manifested CAA secondary (systemic) arterial hypertension, the most common form of parenchymal renal disease and renal vascular lesions. Renovascular diseases are a heterogeneous group of pathologies, which includes atherosclerosis of renal arteries, the most common cause; fibromuscular dysplasia (FMD); other more rare diseases, accompanied by a narrowing of the lumen of the renal vessels. Some authors consider the possibility of including a group of renovascular disease presence of multiple renal arteries. Тhe article presents the clinical cases of secondary hyperaldosteronism, caused by FMD and abnormal amounts of the renal arteries, manifested hypertension and increased levels of aldosterone in the blood. Carrying out a detailed search of the diagnostic determination of the ratio of aldosterone to plasma renin helped eliminate endocrine genesis of the disease and to identify the true cause of aldosteronism.

The extent to which the clinical effects of angiotensin receptor blockers (ARB) are related to ambient renin system activity remains poorly defined. Therefore, we measured blood pressure (BP), large (C1) and small (C2) arterial compliance, systemic vascular resistance (SVR), plasma renin activity (PRA), and the 24-h urinary excretion of sodium (UNaV) and aldosterone before and 1, 2, 4, and 24 h after administration of single doses of placebo, and 5, 20, and 40 mg of the ARB olmesartan medoxomil to 12 unmedicated normotensive subjects. In the basal state, SVR was inversely related to UNaV (r=-0,3,p=0,04); the greater the UNaV, the more vasodilated the subject. Indices of arterial compliance, both C1 (r=-0,32,p=0,03) and C2 (r=-0,35,p=0,02) were inversely related to the basal PRA. Renin also predicted olmesartan-induced changes in C1 (r=0,43,p=0,004) and C2r=0,33,p=0,04). The greater the basal PRA, the less the arterial compliance, and the more compliance improved after olmesartan. Both systolic (p=0,003) and diastolic (pr=-0,414,p=0,012; diastolic BP:r=-0.561,pr=-0,44,p=0,007). Finally, aldosterone excretion fell (sig=0,05) on each dose of olmesartan compared with placebo. We conclude that 1) the inverse relation of UNaV and SVR illustrates the reciprocal role of volume versus constrictor factors in maintaining normal BP; and 2) PRA is a physiologic determinant of arterial compliance in normal individuals and of the response to the ARB olmesartan. Measurement of PRA may help to predict clinical ARB responses in individual subjects.

The object of this study is to evaluate the long-term effects of olmesartan on hypertension and the renin-angiotensin-aldosterone system in hypertensive patients. This study evaluated 26 hypertensive male and female outpatients, 38-69 years of age, with a systolic blood pressure > or = 160 mmHg and/or a diastolic blood pressure > or = 95 mmHg. Oral doses of 5 to 40 mg olmesartan were administered once daily. Blood pressure and renin-angiotensin-aldosterone parameters (plasma renin activity and plasma angiotensin I, II, and aldosterone concentrations) were evaluated at 12-16 weeks, 6 months, and 1 year after the start of olmesartan administration. Systolic and diastolic blood pressures were significantly decreased following the administration of olmesartan. The observed decreases in systolic and diastolic blood pressures after 1 year of treatment were 28.8+/-2.1 mmHg and 15.8+/-1.3 mmHg, respectively. No change was observed in the pulse rate. The plasma renin activity increased significantly from a baseline premedication mean of 1.26+/-0.31 ng/ml/h to a mean of 2.58+/-0.74 ng/ml/h and 2.87+/-0.72 ng/ml/h after 6 months and 1 year of treatment, respectively. Angiotensin II levels decreased significantly from a baseline of 20.4+/-3.2 pg/ml to a mean of 8.6+/-2.1 pg/ml and 6.8+/-1.8 pg/ml after 6 months and 1 year of treatment, respectively. The plasma aldosterone level also decreased significantly after 6 months of treatment. In hypertensive patients, the long-term administration of olmesartan, a novel AT1 receptor antagonist, decreased both blood pressure and plasma angiotensin II levels.

Objective: to study the pathogenetic mechanisms of development of arterial hypertension (AH) in pregnant females and to develop clinical and laboratory criteria that may determine the type of AH in them on the basis of a comprehensive study of hemostatic parameters. Subjects and materials. A hundred and seventy-two pregnant females with AH (a study group) and 54 healthy pregnant ones (a control group) were examined in the third trimester of pregnancy. In all, biochemical blood and urinary analyses determining the concentrations of urea, creatinine, sodium, and protein, followed by the calculation of partial renal functions, were made by the unified method. Enzyme radioimmunoassay was used to determine plasma renin activity. The concentrations of angiotensin-2, aldosterone, thyroxine-binding globulin, testosterone, estriol, estradiol, progesterone, and placental lactogen were measured by enzyme radioimmunoassay. Enzyme immunoassay was employed to estimate the levels of prostanoids. The activity of membranous lipid peroxidation was assessed by the level of its metabolites; the state of the antioxidative system was evaluated. The degree of endogenous intoxication was determined. Central hemodynamic parameters were estimated by tetrapolar rheography. Statistical processing used IBM 384/387 and the statistical package «Stadia». Results. Arterial hypertension caused by pregnancy was ascertained to involve pathogenetical-ly different types: low-, normal-, and high-renin ones. According to its type, the mechanisms of AH were variable. The pressor mechanisms in the pathogenesis of AH were sodium and water retention and elevated total peripheral resistance due to the activation of extrarenal (placental hormonal imbalance, increases in cortisol and angiotensin-2) and renal (increased ARP) pressor systems. The renal depressor system was presented by prostaglandins, the extrarenal depressor system by thyroxine. Conclusion. Activation of the extrarenal depressor system (elevated T4) was common in the pathogenesis of AH in the pregnant females. The knowledge of the pathogenetic mechanisms underlying the development of AH in pregnant females serves as the basis for working out a differential intensive care program.