scholarly journals Polymorphism of the renin-angiotensin system genes and endothelial NO-synthase gene in obese patients with arterial hypertension

2018 ◽  
Vol 34 (5) ◽  
pp. 331-349
Author(s):  
T. V. Ashcheulova ◽  
N. N. Gerasimchuk ◽  
G. V. Demydenko ◽  
M. V. Kulikova
Keyword(s):  
Arterial Hypertension ◽  
Renin Angiotensin System ◽  
No Synthase ◽  
Obese Patients ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Endothelial No Synthase

Intrarenal renin-angiotensin system in hypertensive patients with localized kidney cancer.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e17069-e17069
Author(s):  
Roman Osokin ◽  
Ekaterina Komarova ◽  
Igor Aboyan ◽  
Aleksey Yu. Maksimov ◽  
Roman Ischenko ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Kidney Cancer ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Peritumoral Tissue ◽  
The Relationship ◽  
Angiotensin Converting Enzymes

e17069 Background: In the last decade, the relationship between arterial hypertension and the risk of developing kidney cancer has been pointed out. Some studies have shown that the metabolic imbalance of the components of the renal renin-angiotensin system (RAS) is associated with the development and progression of kidney cancer. Aim: To study the state of RAS in tumor and peritumoral tissues in hypertensive patients with kidney cancer. Methods: In patients with localized kidney cancer T1N0M0 and grade I-II arterial hypertension without special treatment (n = 40; KC + AH) in the samples of tumor (TT), peritumoral (PTT) and histologically unchanged tissue (HUT), the levels of angiotensin 1 and 2, 1-7 (AT1 and AT2, AT (1-7)) of angiotensin-converting enzymes (ACE and ACE2) were determined by ELISA. The comparison group consisted of patients with RC without impaired blood pressure (n = 55, KC). Results: In patients with KC, the level of AT1 is 1.5 times higher (p < 0.05), and AT2 is 1.6 times higher (p < 0.05) in TT against the background of unchanged content in PTT compared with HUT. The level of ACE is higher than HUT by 2.7 times, ACE2 - by 1.6 times (in all cases p < 0.05), and in PTT it is identical in HUT. In patients with KC + AH, the level of AT1 and AT2 in the TT is 1.8 times higher (p < 0.05) and 2.1 times (p < 0.01), respectively, the content of AT(1-7) is 1.6 times (p < 0.01). In PTT, AT1 is 1.6 times higher (p < 0.01) and AT2 is 1.9 times higher (p < 0.05), significantly lower than only AT2 in the TT (1.2 times at p < 0, 05). The level of AT(1-7) in the PTT is identical to the values in the GNT. The content of ACE and ACE2 in TT is 3.6 and 2.9 times higher, respectively, and in PTT is identical to that in TT. Correlation analysis revealed a reliable direct relationship in the studied groups for all parameters, while in the PTT of hypertensive patients, the relationship between the average blood pressure and the RAS peptide content had a higher tightness. Conclusions: An increase in the levels of angiotensin 1 and 2, angiotensin-converting enzymes ACE and ACE2 in the tumor tissues and peritumoral tissue in patients with localized kidney cancer, regardless of the presence of arterial hypertension at initially higher values in hypertensive patients, was shown. The presence of arterial hypertension in patients with KC changes the metabolism of local RAS in peritumoral tissue and is associated with an increase in the correlation between changes in the components of RAS and arterial hypertension.

The serum level of the components of the renin-angiotensin system correlates with its tumor tissue expression in kidney cancer patients.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e17068-e17068
Author(s):  
Roman Osokin ◽  
Ekaterina Komarova ◽  
Igor Aboyan ◽  
Aleksey Yu. Maksimov ◽  
Natalya D. Ushakova ◽  
...  
Keyword(s):  
Arterial Hypertension ◽  
Kidney Cancer ◽  
Peripheral Blood ◽  
Tumor Tissue ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Healthy Donors ◽  
Peritumoral Tissue ◽  
Angiotensin Converting Enzymes

e17068 Background: To date, it has not been decided whether the locally-generated components of the renin-angiotensin system (RAS) involved in the pathogenesis of kidney cancer and arterial hypertension, and are local and systemic RAS related? The aim was to assess the relationship of the level of RAS in the tumor tissue and peripheral blood in patients with localized kidney cancer with arterial hypertension. Methods: In patients with localized kidney cancer T1N0M0 (KС) and arterial hypertension of the I-II stage (AH), tissue and serum levels of angiotensin I, angiotensin II, angiotensin (1-7), as well as angiotensin converting enzymes (ACE and ACE2) were determined in the following groups: patients with KC without AH (n = 35, KC) and with concomitant AH (n = 30; KC+ AH). The normative values of peripheral blood indices were revealed in healthy donors (n = 30). Results: The level of all studied RAS peptides in the serum of patients with KC was increased in comparison with healthy donors regardless of concomitant hypertension, and the activity of both circulating angiotensin-converting enzymes, on the contrary, was increased only in patients with hypertension. The level of AT1 exceeds the control indicators by 1.7 times (KC) and 2.8 times (KC + AH). The formation of AT2 is higher in the KC + AH compared to KC (2.2 times versus 1.7 times, at p < 0.05). The content of AT (1-7) significantly exceeds the control (1.3 times on average, p < 0.05) and higher in the KC + AH. Increased enzyme activity was detected in KC + AG: increased by 1.5 times (p < 0.05) and 1.7 (p < 0.05) compared with the control for ACE and ACE2, respectively. The pair correlation coefficients between the serum RAS and the studied tissues in the KC were: for AT1 -0.78/0.65; АТ2-0.64/0.59 and АТ (1-7) - 0.56/0.51; ACE2 0.55/0.65 (for tumor/peritumoral tissue: in all cases at p < 0.05). In the KC+AH, these ratios were: for AT1 -0.85/0.81; АТ2-0.72/0.74 and АТ (1-7) - 0.65/0.59; ACE2 0.61/0.52 (for tumor / peritumoral tissue: in all cases at p < 0.05). Conclusions: The serum content of RAS peptides had positive statistical relationships with the corresponding parameters in tumor and peritumoral tissues of kidney cancer pts. However, in hypertensive patients with kidney cancer the correlations found had a tightness of higher strength. Positive correlations of the level of locally generated tumor parameters of RAS with their circulating analogues indicate the possibility of their use as diagnostic markers of the development of kidney cancer.

scholarly journals Nebivolol Ameliorates Nitric Oxide–Deficient Hypertension

2002 ◽  
Vol 2 ◽  
pp. 1676-1684 ◽  
Author(s):  
L.A. Fortepiani ◽  
M.C. Ortiz ◽  
N.M. Atucha ◽  
Joaquin Garcia-Estan
Keyword(s):  
Nitric Oxide ◽  
Arterial Hypertension ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
No Synthase ◽  
Nitric Oxide Synthesis ◽  
Synthesis Inhibitor ◽  
Angiotensin System ◽  
Calcium Dependent ◽  
Adrenoceptor Antagonist

Nebivolol is a new selective beta 1-adrenoceptor antagonist with nitric oxide (NO)–releasing properties. In the present study we have analyzed whether nebivolol affects the development of the arterial hypertension that follows the chronic inhibition of nitric oxide synthesis. Nebivolol (1 mg/kg/day, 14 days) was given concurrently with the NO synthesis inhibitor Nw-nitro-L-arginine methyl ester (L-NAME, 0.1, 1, and 10 mg/kg/day, 14 days) to several groups of rats. Blood pressure, renal function, plasma renin activity (PRA), and NO activity and metabolites were measured at the end of the treatment period. L-NAME treatment alone increased mean arterial pressure dose dependently (103.5 ± 2.4, 110.9 ± 2.0, and 125.8 ± 2.2 mmHg, respectively). Nebivolol completely prevented the development of arterial hypertension in the groups treated with L-NAME at the doses of 0.1 and 1 mg/kg/day and reduced the increase achieved with the L-NAME dose of 10 mg/kg/day (110.3 ± 2.7). There were no differences in glomerular filtration rate or natriuresis between nebivolol-treated and -untreated rats. Plasma nitrates+nitrites and calcium-dependent NO synthase activity in the kidney also decreased dose dependently with L-NAME treatment and nebivolol did not significantly modify it. However, PRA was lower in all groups treated with nebivolol and L-NAME as compared to the rats receiving only L-NAME. These data indicate that nebivolol prevents the development of the arterial hypertension associated with chronic NO deficit and this effect seems to be dependent on the inhibition of renin-angiotensin system.

Role of the Renin—Angiotensin System in Arterial Hypertension Secondary to Acute Unilateral Urinary Obstruction

Renal Failure ◽  
1994 ◽  
Vol 16 (6) ◽  
pp. 673-679 ◽  
Author(s):  
G. Hernández-Llamas ◽  
G. Palafox-Cervantes ◽  
Alma L. Borboa-Osuna ◽  
J. Urrecha-Manzano ◽  
C. Cruz ◽  
...  
Keyword(s):  
Arterial Hypertension ◽  
Renin Angiotensin System ◽  
Urinary Obstruction ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Obesity, Renin-Angiotensin System Blockade and Risk of Adverse Renal Outcomes: A Population-Based Cohort Study

2016 ◽  
Vol 43 (6) ◽  
pp. 431-440 ◽  
Author(s):  
Jordana B. Cohen ◽  
Alisa J. Stephens-Shields ◽  
Michelle R. Denburg ◽  
Amanda H. Anderson ◽  
Raymond R. Townsend ◽  
...  
Keyword(s):  
Cohort Study ◽  
Renin Angiotensin System ◽  
Structural Modeling ◽  
Diabetic Patients ◽  
Obese Patients ◽  
Antihypertensive Medications ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Outcomes ◽  
Marginal Structural Modeling

Background: Obesity substantially increases the risk of the development of chronic kidney disease. Adipose tissue expresses all of the components of the renin-angiotensin system (RAS), contributing to the high prevalence of hypertension in obese patients and driving renal hyperfiltration and subsequent glomerular injury. Methods: We performed a retrospective cohort study using a United Kingdom primary care database, evaluating the effect of time-updated exposure to RAS blockade versus all other antihypertensive medications in obese, hypertensive, non-diabetic patients. We used Cox proportional hazards modeling with and without marginal structural modeling to assess the hazards of developing a primary outcome of 50% reduction in estimated glomerular filtration rate (eGFR) (across 2 consecutive values), end stage renal disease or death. Results: A total of 219,701 patients met inclusion criteria, with a median 7.2 years of follow-up. Median baseline eGFR was 72.6 ml/min/1.73 m2. Compared to other antihypertensive medications, patients treated with RAS blockade had a modestly elevated hazard of adverse renal outcomes using traditional Cox regression (hazard ratio (HR) 1.04, 95% CI 1.01-1.07) and no significantly increased hazard by marginal structural modeling (HR 1.02, 95% CI 0.97-1.08). Patients treated with RAS blockade had a significantly reduced hazard of incident diabetes, but no significant difference in mortality. Conclusion: This study, conducted in a large real-world cohort, provides evidence that RAS blockade may not provide benefit with regard to longitudinal renal outcomes in obese, hypertensive patients. Further research is needed to elucidate the hemodynamic and renoprotective role of antihypertensive medications in obese patients.

scholarly journals Genetics and pathophysiology of low-renin arterial hypertension

2019 ◽  
Vol 22 (8) ◽  
pp. 1000-1008 ◽  
Author(s):  
A. L. Markel
Keyword(s):  
Arterial Hypertension ◽  
Molecular Genetic ◽  
Renin Angiotensin System ◽  
Hypertensive Disease ◽  
Genetic Determination ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Family Analysis ◽  
Low Renin Hypertension ◽  
Key Enzyme

The review is devoted to the consideration of genetic determination and pathophysiology of one of the forms of hypertensive disease known as low-renin hypertension. At frst glance, the development of low-renin hypertension is “unnatural”, as renin, as a key enzyme of the renin-angiotensin system, which plays an important role in the development of hypertensive disease, is suppressed in low-renin hypertension. At the same time, the most important drugs actual in the treatment of hypertensive disease belong to the renin-angiotensin system blockers. This contradiction was resolved by a study of genetic and pathophysiological mechanisms of hypertension in some groups of patients with characteristic symptoms bringing these people together. Genetic studies of some recent decades using both family analysis and modern molecular genetic technologies have revealed the main mechanisms underlying low-renin hypertension, which can be classifed as certain syndromes with well-defned genetic and clinical features. These syndromes include cases of sporadically occurring somatic mutations in the cells of the adrenal cortex, which begin to produce aldosterone in increased amounts. Also, several oligogenic forms of low-renin hypertension were studied, some of which are associated with the hyperproduction of aldosterone, but in the others the development of low-renin hypertension was associated with mutations of genes involved in regulation of the functioning of the kidney ion channels. The discovery of some types of arterial hypertension with known mechanisms of their development is of paramount importance for medicine, as it allows for targeted efective therapy and in some cases for achieving a complete cure. However, the main contingent of patients with low-renin hypertension belongs to cases with unexplained etiology, as their development is associated with polygenic systems and with a signifcant influence of numerous environmental factors. The study of genetic and physiological mechanisms of various forms of low-renin arterial hypertension provides a good example of how penetration into the intimate mechanisms of the blood pressure regulation in each personal case makes it possible to identify some specifc syndromes and establish its fnal causes. It seems that progress in understanding the causes and mechanisms of essential hypertension lies along this way.

scholarly journals Tissue synthesis of some components of the renin-angiotensin system in hypertensive patients with localized kidney cancer

2020 ◽  
Vol 16 (1) ◽  
pp. 27-34
Author(s):  
R. A. Osokin ◽  
I. A. Aboyan ◽  
E. F. Komarova ◽  
A. Yu. Maksimov ◽  
E. Yu. Komarova
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Kidney Cancer ◽  
Tumor Tissue ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Peritumoral Tissue ◽  
The Relationship

Background. In the last decade, the relationship between arterial hypertension and the risk of developing kidney cancer (KC) has been pointed out. Some studies have shown that the metabolic imbalance of the components of the renal renin-angiotensin system (RAS) is associated with the development and progression of KC.Objective: to study the state of RAS in tumor and peritumoral tissues in patients with KC on the background of arterial hypertension. Materials and methods. In patients with localized KC T1N0M0 and grade I–II arterial hypertension without special treatment (n = 40) in the samples of tumor, peritumoral and histologically unchanged tissue, the levels of angiotensins 1, 2, 1–7 (AT1, AT2, AT(1–7)) of angiotensin-converting enzymes (ACE, ACE2) were determined by ELISA. The comparison group consisted of patients with RC without impaired blood pressure (n = 55).Results. In patients with KC, the level of AT1 is 1.5 times higher (p <0.05), and AT2 is 1.6 times higher (p <0.05) in tumor tissue against the background of unchanged content in peritumoral tissue compared with histologically unchanged tissue. The level of ACE is higher than histologically unchanged tissue by 2.7 times, ACE2 – by 1.6 times (in all cases p <0.05), and in peritumoral tissue it is identical in histologically unchanged tissue.In patients with KC and arterial hypertension, the level of AT1 and AT2 in the tumor tissue is 1.8 times higher (p <0.05) and 2.1 times (p <0.01), respectively, the content of AT(1–7) is 1.6 times (p <0.01). In peritumoral tissue, AT1 is 1.6 times higher (p <0.01) and AT2 is 1.9 times higher (p <0.05). The level of AT(1–7) in the peritumoral tissue is identical to the values in the histologically unchanged tissue. The content of ACE and ACE2 in tumor tissue is 3.6 and 2.9 times higher, respectively, and in peritumoral tissue is identical to that in tumor tissue. Correlation analysis revealed a reliable direct relationship in the studied groups for all parameters, while in the peritumoral tissue of hypertensive patients, the relationship between the average blood pressure and the RAS peptide and enzymes content had a higher tightness.Conclusion. An increase in the levels of AT1 and AT2, ACE and ACE2 in the tumor tissues and peritumoral tissue in patients with localized KC, regardless of the presence of arterial hypertension at initially higher values in hypertensive patients, was shown. The presence of arterial hypertension in patients with KC changes the metabolism of local RAS in peritumoral tissue and is associated with an increase in the correlation between changes in the components of RAS and arterial hypertension.

Mesenchymal stem cell–derived microvesicles alleviate pulmonary arterial hypertension by regulating renin-angiotensin system

2018 ◽  
Vol 12 (6) ◽  
pp. 470-478 ◽  
Author(s):  
Zhenjun Liu ◽  
Jinghu Liu ◽  
Mengyuan Xiao ◽  
Junxian Wang ◽  
Feng Yao ◽  
...  
Keyword(s):  
Stem Cell ◽  
Pulmonary Arterial Hypertension ◽  
Mesenchymal Stem Cell ◽  
Arterial Hypertension ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Pulmonary Arterial
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