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To measure the concentration of plasma soluble angiotensin IV receptor (sAT-4), a component of the renin-angiotensin system in healthy normotensive pregnancies and preeclampsia. Stored maternal plasma samples obtained at the time of diagnosis from pregnant women of African ancestry were stratified into normotensive and preeclampsia groups. Preeclampsia was subdivided into early-onset, late-onset, and into and severe preeclampsia. Plasma concentrations of sAT-4 were measured at 450 nm using the ELISA technique (LNPEP KIT). The systolic and diastolic blood pressure (BP) levels of the normotensive group were statistically lower compared to preeclampsia groups (p <.05) and the mean gestational age in early-onset preeclampsia was lower compared to late-onset preeclampsia and the normotensive group (p <.05). Plasma sAT-4 levels were significantly elevated (p <.0001) in the normotensive group (median 1.95, range 1.89–2.02 ng/ml) compared to the preeclampsia group (median 1.55, range 1.42–1.74 ng/ml), regardless of gestational age. Soluble AT-4 was decreased in relation to the severity of preeclampsia (p <.001), the level in preeclampsia without severe features (median 1.57, range 1.42–1.74 ng/ml) was significantly higher than in preeclampsia with severe features (median 1.51, range 1.42–1.55 ng/ml). There was no significant difference in the sAT-4 level between early-onset preeclampsia (1.60 ± 0.13 ng/ml) and late-onset preeclampsia (1.65 ± 0.29 ng/ml) groups (p =.59). Plasma circulating levels of sAT-4 in women with severe features of preeclampsia had lower levels than normotensives and those with preeclampsia without severe features. [ABSTRACT FROM AUTHOR]

A growing body of evidence highlights that several insults during pregnancy impact the vascular function and immune response of the male and female offspring. Overactivation of the immune system negatively influences cardiovascular function and contributes to cardiovascular disease. In this review, we propose that modulation of the immune system is a potential link between prenatal stress and offspring vascular dysfunction. Glucocorticoids are key mediators of stress and modulate the inflammatory response. The potential mechanisms whereby prenatal stress negatively impacts vascular function in the offspring, including poor hypothalamic–pituitary–adrenal axis regulation of inflammatory response, activation of Th17 cells, renin–angiotensin–aldosterone system hyperactivation, reactive oxygen species imbalance, generation of neoantigens and TLR4 activation, are discussed. Alterations in the immune system by maternal stress during pregnancy have broad relevance for vascular dysfunction and immune-mediated diseases, such as cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background The effects of sodium (Na+) intakes on renal handling of potassium (K+) are insufficiently studied. Methods We assessed the effect of Na+ on renal K+ handling in 16 healthy males assigned to three 7-day periods on low salt diet [LSD, 3 g sodium chloride (NaCl)/day], normal salt diet (NSD, 6 g NaCl/day) and high salt diet (HSD, 15 g NaCl/day), with constant K+ intake. Contributions of distal NaCl co-transporter and epithelial Na+ channel in the collecting system on K+ and Na+ handling were assessed at steady state by acute response to 100 mg oral hydrochlorothiazide and with addition of 10 mg of amiloride to hydrochlorothiazide, respectively. Results Diurnal blood pressure slightly increased from 119.30 ± 7.95 mmHg under LSD to 123.00 ± 7.50 mmHg (P = 0.02) under HSD, while estimated glomerular filtration rate increased from 133.20 ± 34.68 mL/min under LSD to 187.00 ± 49.10 under HSD (P = 0.005). The 24-h K+ excretion remained stable on all Na+ intakes (66.28 ± 19.12 mmol/24 h under LSD; 55.91 ± 21.17 mmol/24 h under NSD; and 66.81 ± 20.72 under HSD, P   =   0.9). The hydrochlorothiazide-induced natriuresis was the highest under HSD (30.22 ± 12.53 mmol/h) and the lowest under LSD (15.38 ± 8.94 mmol/h, P   =   0.02). Hydrochlorothiazide increased kaliuresis and amiloride decreased kaliuresis similarly on all three diets. Conclusions Neither spontaneous nor diuretic-induced K+ excretion was influenced by Na+ intake in healthy male subjects. However, the respective contribution of the distal convoluted tubule and the collecting duct to renal Na+ handling was dependent on dietary Na+ intake. [ABSTRACT FROM AUTHOR]

Background: For the Asian patients with STEMI undergoing PCI, ACEIs are known to have a better outcome than ARBs. However, there is limited evidence to suggest so.Methods: Among the STEMI registry consist of 1142 Korean patients, we compared the MACE, the composite of myocardial infarction, stoke, death, admission for heart failure, and target vessel revascularization, between the ACEI and ARB groups (Set 1). Further, we defined adequate medication as the administration of a dose equal to or higher than the initiation dose of ACEI according to the heart failure guideline recommendation with a mandatory addition of beta-blockers, and compared the outcomes between the inadequate and adequate medication groups (Set 2). Propensity score matching was used to eliminate difference.Results: In the Set 1 comparison, patients in the ACEI group had a better outcome than those in the ARB group for both whole and matched populations (whole and matched population: Cox regression hazard ratio [HR], 0.645 and 0.535; 95% confidence interval [CI], 0.440-0.944 and 0.296-0.967; p = 0.024 and p = 0.039, respectively). In the Set 2 comparison for the whole population, patients in the inadequate medication group had more MACE than those in the adequate medication group (HR, 0.673; 95% CI, 0.459-0.985; p = 0.042). However, no difference was observed after propensity score matching (HR, 1.023; 95% CI, 0.654-1.602; p = 0.919).Conclusion: ACEIs might be a better choice than ARBs after primary revascularization. However, this study's findings suggest that early ACEI dose escalation combined with beta-blocker use may not improve prognosis. [ABSTRACT FROM AUTHOR]

Background: During pregnancy, the renin–angiotensin–aldosterone system (RAAS) undergoes major changes to preserve normal blood pressure (BP) and placental blood flow and to ensure a good pregnancy outcome. Abnormal aldosterone–renin metabolism is a risk factor for arterial hypertension and cardiovascular risk, but its association with pathological conditions in pregnancy remains unknown. Moreover, potential biomarkers associated with these pathological conditions should be identified. Aim: To study a cohort of normotensive pregnant women according to their serum aldosterone and plasma renin levels and assay their small extracellular vesicles (sEVs) and a specific protein cargo (LCN2, AT1R). Methods: A cohort of 54 normotensive pregnant women at term gestation was included. We determined the BP, serum aldosterone, and plasma renin concentrations. In a subgroup, we isolated their plasma sEVs and semiquantitated two EV proteins (AT1R and LCN2). Results: We set a normal range of aldosterone and renin based on the interquartile range. We identified 5/54 (9%) pregnant women with elevated aldosterone and low renin levels and 5/54 (9%) other pregnant women with low aldosterone and elevated renin levels. No differences were found in sEV-LCN2 or sEV-AT1R. Conclusion: We found that 18% of normotensive pregnant women had either high aldosterone or high renin levels, suggesting a subclinical status similar to primary aldosteronism or hyperreninemia, respectively. Both could evolve to pathological conditions by affecting the maternal vascular and renal physiology and further the BP. sEVs and their specific cargo should be further studied to clarify their role as potential biomarkers of RAAS alterations in pregnant women. [ABSTRACT FROM AUTHOR]

Aim. To study the dependence of the effectiveness of antihypertensive therapy on the polymorphic variants of candidate genes of the RAAS (ACE, AGT, AGTR1) in patients with hypertension (АH) of the population of Mountain Shoria. Materials and methods. In the conditions of the expeditions from 2013 to 2017, the population of Mountain Shoria was surveyed. Included 1409 people 18 years and older. Blood pressure monitoring was carried out as a result of office measurement, according to the standard recommendations of National Guidelines of the Russian Society of Cardiology/the Russian Medical Society on Arterial Hypertension (2010). As a result of the survey, patients with AH were identified for further observation (597 people) who need medical antihypertensive treatment. Repeat screening was conducted in a year. The criterion for inclusion in prospective observation of patients with hypertension was: regular intake of prescribed medication. 253 respondents were surveyed: indigenous (156 people) and non-indigenous (97 people) nationality. All patients underwent a standard examination, including the collection of complaints and anamnesis, an assessment of objective status, laboratory and instrumental studies. Polymorphisms of genes ACE (I/D, rs 4340), AGT (c.803T C, rs699), AGTR1 (A1166C, rs5186) were tested using polymerase chain reaction. Results. Dynamic observation of patients with hypertension found that in the cohort of Shors the target level of blood pressure reached the owners of heterozygous I/D and minor D/D genotypes of the ACE gene, carriers of T/C and C/C genotypes of the AGT gene and the homozygous genotype A/A of the AGTR1 gene. In the non-indigenous nationality cohort, only carriers of the D/D genotype of the ACE gene. Conclusion. National differences were identified with respect to the sensitivity of the pharmacological response to treatment, which once again proves the important role of taking into account the ethnic factor in the choice of drug.

Background/Purpose: Chronic kidney disease (CKD) is a risk factor for contrast associated acute kidney injury (CA-AKI). The risk of renin-angiotensin-aldosterone system inhibitor (RASi) use in patients with CKD before the administration of contrast is not clear. Methods: In this nested case–control study, 8668 patients received contrast computed tomography (CT) from 2013 to 2018 during index administration in a multicenter hospital cohort. The identification of AKI is based on the Kidney Disease: Improving Global Outcomes (KDIGO) serum creatinine criteria within 48 h after contrast medium used. Results: Finally, 986 patients (age, 63.36 ± 12.22; men, 72.92%) with CKD (estimated glomerular filtration rate (eGFR) = 35.0 ± 19.8 mL/min/1.73 m2) were eligible for analysis. After the index date, RASi users (n = 315) were less likely to develop CA-AKI (13.65% vs 30.4%, p

Abstract Background Several large clinical trials have confirmed the cardioprotective role of sodium-glucose cotransporter 2 inhibitors (SGLT2i) in patients with type 2 diabetes. However, whether empagliflozin, as an SGLT2i, could alleviate atherosclerosis progression in non-diabetic states remain unknown. Methods ApoE-/- mice were fed a Western diet for 12 weeks to induce atherosclerosis. On the 7th week, a group of mice were treated with drinking water containing empagliflozin (10 mg/kg/day), while another group was given normal water. At the 12th week, the whole aortas of each group were harvested. Oil Red O, HE and Movat staining were performed for atherosclerotic lesion area and size. Mouse serum lipid profiles (total cholesterol [TC], triglyceride [TG], low-density lipoprotein-c [LDL], and high-density lipoprotein-c [HDL]), systemic inflammation levels (IL-1β, IL-6 and IL-10), renin-angiotensin-aldosterone system (RAAS) components and sympathetic activity (norepinephrine and neuropeptide Y) indicators were measured by ELISA. Results Empagliflozin reduced the atherosclerotic lesion burden (-8.6 %, P = 0.004) at aortic root in ApoE-/- mice. In addition, empagliflozin decreased body weight (-3.27 g, P = 0.002), lipid profiles (TC: [-15.3 mmol/L, P = 0.011]; TG: [-2.4 mmol/L, P

Abstract Background To investigate the effects of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin receptor blockers (ARBs) administration to hypertension patients with the coronavirus disease 2019 (COVID-19) induced pneumonia. Methods We recorded the recovery status of 67 inpatients with hypertension and COVID-19 induced pneumonia in the Raytheon Mountain Hospital in Wuhan during February 12, 2020 and March 30, 2020. Patients treated with ACEI or ARBs were categorized in group A (n = 22), while patients who were not administered either ACEI or ARBs were categorized into group B (n = 45). We did a comparative analysis of various parameters such as the pneumonia progression, length-of-stay in the hospital, and the level of alanine aminotransferase (ALT), serum creatinine (Cr), and creatine kinase (CK) between the day when these patients were admitted to the hospital and the day when the treatment ended. Results These 67 hypertension cases counted for 33.17% of the total COVID-19 patients. There was no significant difference in the usage of drug treatment of COVID-19 between groups A and B (p > 0.05). During the treatment, 1 case in group A and 3 cases in group B progressed from mild pneumonia into severe pneumonia. Eventually, all patients were cured and discharged after treatment, and no recurrence of COVID-2019 induced pneumonia occurred after the discharge. The length of stays was shorter in group A as compared with group B, but there was no significant difference (p > 0.05). There was also no significant difference in other general parameters between the patients of the groups A and B on the day of admission to the hospital (p > 0.05). The ALT, CK, and Cr levels did not significantly differ between groups A and B on the day of admission and the day of discharge (p > 0.05). Conclusions To treat the hypertension patients with COVID-19 caused pneumonia, anti-hypertensive drugs (ACEs and ARBs) may be used according to the relative guidelines. The treatment regimen with these drugs does not need to be altered for the COVID-19 patients.

Numerous reports have suggested that diabetic patients are at high risk for the development of severe symptoms of coronavirus disease-2019 (COVID-19). However, a few studies have recently proposed that the relationship between diabetes and COVID-19 is bidirectional, as severe acute respiratory syndrome-coronavirus-2 also has the capability to induce diabetes. Various mechanisms have been identified and proposed to be involved in this binary association. In this review, the importance and impact of renin–angiotensin–aldosterone system (RAAS) in this two-way association of COVID-19 and diabetes has been summarized. The role and effect of drugs modulating RAAS directly or indirectly has also been discussed, as they can majorly impact the course of treatment in such patients. Further reports and data can present a clear picture of RAAS and its modulators in restoring the balance of dysregulated RAAS in COVID-19.

In the development of renocardial relationships in chronic kidney disease, an important role is given to the activation of the renin-angiotensin-aldosterone system (RAAS), as the main component of the progression and development of cardiovascular complications..The presented review is devoted to the analysis of modern scientific data on the effect of high RAAS activity in chronic kidney disease on the course and prognosis of cardiovascular complications, as well as the protective capabilities of angiotensin-converting enzyme inhibitors, in particular perindopril. The results of scientific research on the role of the RAAS in the progression of chronic kidney disease are summarized. Data on chronic kidney disease as a risk factor for cardiovascular and cerebral complications are presented. Attention is focused on the possibilities of prolonging the pre-dialysis period of chronic kidney disease when using angiotensin-converting enzyme inhibitors. The role of perindopril as a lipophilic angiotensin-converting enzyme inhibitor with a high affinity for tissue RAAS was emphasized in reducing cardiovascular and cerebral risk in chronic kidney disease.

Objective: to evaluate the effect of renin-angiotensin-aldosterone system (RAAS) blockers on aldosterone level in patients with chronic heart failure with preserved ejection fraction (HFpEF).Materials and methods: the prospective study included 158 patients (58 men and 100 women, mean age 62,3 ± 7,4 years) with HFpEF (> 50 %) and left ventricular diastolic dysfunction. All patients had no history of primary aldosteronism and did not use the mineralocorticoid receptor antagonists during the last 6 weeks. We evaluated the duration of treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin-2 receptor antagonists (ARA-2) and its average daily dose. The dose of RAAS blockers was assessed during previous 6 months as a percentage of target. Aldosterone plasma concentration was measured and the normal level was 40 – 160 pg/ml.Results: according to laboratory results 99 patients (62,7 %) had normal aldosterone level (nAld) and 59 patients (37,3 %) had high aldosterone level (hAld). hAld patients had significantly higher duration of RAAS blockers treatment (6 (3; 8) versus 4 (2; 5) years, p < 0,001) and dose (50 (25; 50) % vs 25 (12,5; 50) % of target, р=0,01). Multiple regression analysis showed that after standartization for age, severity of HFpEF, duration of arterial hypertension and comorbidity only long-term (more than 5 years) treatment with RAAS blockers remained the independent risk factor of high aldosterone level (odds ratio 3,16, 95 % confidence interval 2,08 – 8,24).Conclusions: in HFpEF patients’ plasma aldosterone level is closely associated with RAAS blockers treatment. Long-term (more than 5 years) therapy with ACE inhibitors or ARA-2 is the independent risk factor of secondary hyperaldosteronism.

Abstract People with cardiovascular disease (CVD) often contract coronavirus disease 2019 (COVID‐19). However, the interaction between COVID‐19 and CVD is unclear. In this systematic review, the available evidence for the crosstalk between COVID‐19 and CVD and its treatment was analysed. A search was performed in the electronic databases MEDLINE and EMBASE. Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infects human cells via angiotensin‐converting enzyme 2. SARS‐CoV‐2 can cause CVD by inducing cytokine storms, creating an imbalance in the oxygen supply and demand and disrupting the renin–angiotensin–aldosterone system; SARS‐CoV‐2 infection can also lead to the development of CVD through the side effects of therapeutic drugs, psychological factors, and aggravation of underlying CVD. The most common CVDs caused by SARS‐CoV‐2 infection are acute myocardial injury, arrhythmia, and heart failure. Studies have found that there is an interaction between COVID‐19 and CVD. Underlying CVD is associated with a high risk of mortality in patients with COVID‐19. SARS‐CoV‐2 infection can also cause new‐onset CVD. Clinicians need to pay close attention to cardiovascular complications during the diagnosis and treatment of patients with COVID‐19 to reduce patient mortality.

BackgroundCardiac rehabilitation (CR) is recommended for patients with acute heart failure (HF). However, the results of outcome studies and meta-analyses on CR in post-acute care are varied. We aimed to assess the medium- to long-term impact of CR and ascertain the predictors of successful CR.MethodsIn this propensity score-matched retrospective cohort study, records of consecutive patients who survived acute HF (left ventricular ejection fraction

BackgroundSarcopenia is related to morbidity and mortality in non-dialysis Chronic Kidney Disease (ND-CKD) patients; however, the pathophysiology of sarcopenia remains unclear. The study aimed to assess the prevalence and factors associated with sarcopenia in ND-CKD individuals.MethodsWe cross-sectionally evaluated 139 prevalent ND-CKD patients attending our outpatient clinic at Hospital das Clínicas of the Federal University of Pernambuco, between April and October 2019. Patients older than 18 years old and at G3-G5 CKD stages were included. Hand grip strength, Muscle Mass appendicular Index, and Gait Speed (GS) were defined by the standards of the European Working Group on Sarcopenia in Older People 2 guideline.ResultsSarcopenia prevalence was 20.9% and severe sarcopenia 2.9%. Sarcopenic were mostly found in elderly ones (64.8 ± 13.5 years vs. 54.9 ± 12.8 years, p < 0.001), revealing lower body mass index [26.1 (6.8) vs. 28.6 (6.2), p = 0.023], lower phase angle (PhA) [4.50 (1.10) vs. 5.60 (1.20), p < 0.001] and lower GS [1.00 (0.50) vs. 1.40 (0.4), p < 0.001]. They also presented lower serum creatinine levels [2.40 (1.50) vs. 3.0 (1.8), p = 0.032], lower Albumin-to-Creatinine Ratio [72.60 (1008.30) vs. 342.30 (1172.1), p = 0.039] and Hemoglobin levels [11.45 (1.8) vs. 12.60 (2.40), p = 0.003], and higher levels of C-reactive protein [0.2 (0.80) vs. 0.03 (0.3), p = 0.045] compared to non-sarcopenic. Under Poisson Multivariate Model, PhA [Relative precision (RP): 0.364, Confidence Interval (CI) (95%):0.259–0.511, p < 0.001], Interleukin six (IL-6) [RP: 1.006, CI (95%):1.001–1.01, p = 0.02] and serum creatinine levels [RP: 0.788, CI (95%): 0.641–0.969, p = 0.024] were associated with sarcopenia.ConclusionsSarcopenia predominance was identified in our ND-CKD population, and was associated with lower PhA values, higher IL-6 levels, and lower serum creatinine levels.

The assessment of systemic corticosteroid effects on intrapulmonary disease biomarkers is challenging. This retrospective evaluation of a human endotoxemia model quantified ACE2 and fibrin degradation product (FDP) concentrations in bronchoalveolar lavage fluid (BALF) samples from a randomized, double-blind, placebo-controlled study (NCT01714427). Twenty-four healthy volunteers received either 2 × 40 mg intravenous dexamethasone or placebo. These doses were administered 12 h apart prior to bronchoscopy-guided intrabronchial lipopolysaccharide (LPS) stimulation (control: saline into the contralateral lung segment). We quantified ACE2 concentration, the Angiotensin-II-to-Angiotensin-1-7 conversion rate as well as FDP in BALF 6 h after LPS instillation. In placebo-treated subjects, LPS instillation increased ACE2 concentrations compared to unstimulated lung segments [1,481 (IQR: 736–1,965) vs. 546 (413–988) pg/mL; p = 0.016]. Dexamethasone abolished the increase in ACE2 concentrations (p=0.13). Accordingly, LPS instillation increased the Angiotensin-II-to-Angiotensin-1-7 conversion capacity significantly in the placebo cohort, indicating increased enzymatic activity (p = 0.012). FDP increased following LPS-instillation [8.9 (2.7–12.2) vs. 6.6 (0.9–9.6) ng/mL, p = 0.025] in the placebo group, while dexamethasone caused a shut-down of fibrinolysis in both lung segments. LPS instillation increased ACE2 concentration, its enzymatic activity and FDP, which was mitigated by systemic dexamethasone treatment. Our results strengthen previously published findings regarding the efficiency of corticosteroids for the treatment of COVID-19-induced acute lung injury.

A growing body of evidence highlights that several insults during pregnancy impact the vascular function and immune response of the male and female offspring. Overactivation of the immune system negatively influences cardiovascular function and contributes to cardiovascular disease. In this review, we propose that modulation of the immune system is a potential link between prenatal stress and offspring vascular dysfunction. Glucocorticoids are key mediators of stress and modulate the inflammatory response. The potential mechanisms whereby prenatal stress negatively impacts vascular function in the offspring, including poor hypothalamic–pituitary–adrenal axis regulation of inflammatory response, activation of Th17 cells, renin–angiotensin–aldosterone system hyperactivation, reactive oxygen species imbalance, generation of neoantigens and TLR4 activation, are discussed. Alterations in the immune system by maternal stress during pregnancy have broad relevance for vascular dysfunction and immune-mediated diseases, such as cardiovascular disease.

In December 2019, the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) rapidly spread to become a pandemic. To date, increasing evidence has described the potential negative impact of SARS-CoV-2 infection on pregnant women. Although the pathophysiology of coronavirus disease 2019 (COVID-19) is not entirely understood, there is emerging evidence that it causes a severe systemic inflammatory response associated with vascular alterations that could be of special interest considering some physiological changes in pregnancy. Additionally, these alterations may affect the physiology of the placenta and are associated with pregnancy complications and abnormal histologic findings. On the other hand, data about the vaccine against SARS-CoV-2 are limited, but the risks of administering COVID-19 vaccines during pregnancy appear to be minimal. This review summarizes the current literature on SARSCoV2 virus infection, the development of COVID-19 and its relationship with physiological changes, and angiotensin-converting enzyme 2 (ACE2) function during pregnancy. We have particularly emphasized evidence coming from Latin American countries.

There is increasing evidence that vitamin D deficiency may contribute to hypertension. Low vitamin D levels are associated with an increased risk of high blood pressure, and studies have shown that vitamin D supplementation can help lower blood pressure. However, more research is needed to fully understand the mechanisms by which vitamin D regulates blood pressure and to determine the optimal dosage for supplementation. Nevertheless, ensuring adequate vitamin D levels through diet or supplements may be essential for preventing and managing hypertension. [ABSTRACT FROM AUTHOR]

The important renal endocrine aspect implicated in gym nephropathy is the activation of the renin-angiotensin-aldosterone system (RAAS). Intense exercise can lead to increased sympathetic nervous system activity, resulting in the release of renin from the juxtaglomerular cells in the kidneys. Renin acts on angiotensinogen, leading to the generation of angiotensin II, a potent vasoconstrictor. Angiotensin II stimulates the secretion of aldosterone from the adrenal glands, which promotes sodium reabsorption and potassium excretion in the kidneys. The persistent activation of the RAAS in gym nephropathy may contribute to renal damage by causing vasoconstriction and promoting renal inflammation. [ABSTRACT FROM AUTHOR]

• Prurigo nodularis (PN) is strongly associated with various renal comorbidities. • Association with renal comorbidities is stronger in black patients. • There is systemic and cutaneous dysregulation of the renin-angiotensin-aldosterone system (RAAS) in PN. • Dysregulation of the RAAS is stronger in black patients with prurigo nodularis. There are limited data characterizing the association between renal disease and prurigo nodularis (PN). To characterize the association and describe mechanistic disease linkages between PN and renal comorbidities. We conducted a cross-sectional analysis of renal comorbidities in PN using TriNetX, a global health research network providing access to medical records. Epidemiological findings provided the basis for translational studies on plasma and skin biopsy samples from PN patients stratified by race. PN was associated with stages 1–5 of chronic kidney disease (CKD), end-stage renal disease, nephritic syndrome, nephrotic syndrome, glomerular disease, and tubulointerstitial disease, but the associations were significantly stronger in black patients. Compared to controls, CKD progression was faster (HR 2.88, 95% CI: 1.01–8.26) only in black PN (10-year survival: 63.5% black vs. 85.5% white). Circulating plasma angiotensinogen levels were dysregulated (P < 0.001) only in black PN patients. Cutaneous transcriptomic analysis of genes related to the renin-angiotensin-aldosterone system (RAAS) revealed considerable dysregulation in PN lesions with greater dysregulation in black patients. Significant dysregulation of the cutaneous and systemic RAAS in black PN patients may explain the increased incidence and severity of renal disease. [ABSTRACT FROM AUTHOR]

SARS‐CoV‐2 interacting with its receptor, angiotensin‐converting enzyme 2 (ACE2), turns the host response to viral infection into a dysregulated uncontrolled inflammatory response. This is because ACE2 limits the production of the peptide angiotensin II (Ang II) and SARS‐CoV‐2, through the destruction of ACE2, allows the uncontrolled production of Ang II. Recovery from trauma requires activation of both a tissue response to injury and activation of a whole‐body response to maintain tissue perfusion. Tissue and circulating renin‐angiotensin systems (RASs) play an essential role in the host response to infection and injury because of the actions of Ang II, mediated via its AT1 receptor. Both tissue and circulating arms of the renin angiotensin aldosterone system's (RAAS) response to injury need to be regulated. The effects of Ang II and the steroid hormone, aldosterone, on fluid and electrolyte homeostasis and on the circulation are controlled by elaborate feedback networks that respond to alterations in the composition and volume of fluids within the circulatory system. The role of Ang II in the tissue response to injury is however, controlled mainly by its metabolism and conversion to Ang‐(1‐7) by the enzyme ACE2. Ang‐(1‐7) has effects that are contrary to Ang II‐AT1R mediated effects. Thus, destruction of ACE2 by SARS‐CoV‐2 results in loss of control of the pro‐inflammatory actions of Ang II and tissue destruction. Therefore, it is the response of the host to SARS‐CoV‐2 that is responsible for the pathogenesis of COVID‐19. [ABSTRACT FROM AUTHOR]

Sodium‐glucose co‐transporter 2 inhibitors (SGLT2‐Is) have emerged as a promising class of antidiabetic drugs with cardioprotective and renoprotective effects in patients with type 2 diabetes (T2D). The sodium‐glucose co‐transporters 1 and 2 (SGLT 1 and SGLT2) located in the renal proximal tubules are responsible for glucose reabsorption from the glomerular filtrate back into the systemic circulation. Inhibition of SGLT2, which accounts for about 90% of the glucose reabsorption, leads to a significant reduction in blood glucose levels and a concomitant increase in the urinary excretion of glucose (glycosuria). Multiple mechanisms contribute to the nephroprotective effects of SGLT2‐Is in T2D patients. These include: (1) Restoration of the tubuloglomerular feedback by increasing sodium delivery at macula densa, leading to afferent arteriolar constriction and reduced glomerular hyperfiltration, (2) Decreased activation of the intra‐renal renin‐angiotensin‐aldosterone system, which also contributes to reducing glomerular hyperfiltration, (3) Increased production of ketone bodies, which serves as an alternate fuel for adenosine triphosphate production in mitochondria, which helps in attenuating inflammation, and (4) Protection against hypoxia, oxidative stress, and fibrosis. This review elaborates on the key mechanisms that underlie the nephroprotective effects and the adverse effects of SGLT2‐Is in T2D patients with progressive diabetic kidney disease. [ABSTRACT FROM AUTHOR]

Superimposed preeclampsia complicates about 20% of pregnancies in women with chronic hypertension and is associated with increased maternal and perinatal morbidity compared with preeclampsia alone. Distinguishing superimposed preeclampsia from chronic hypertension can be challenging because, in chronic hypertension, the traditional criteria for the diagnosis of preeclampsia, hypertension, and significant proteinuria can often predate the pregnancy. Furthermore, the prevalence of superimposed preeclampsia is unlikely to be uniformly distributed across this high-risk group but is related to the severity of preexisting endothelial dysfunction. This has led to interest in identifying biomarkers that could help in screening and diagnosis of superimposed preeclampsia and in the stratification of risk in women with chronic hypertension. Elevated levels of uric acid and suppression of other renal biomarkers, such as the renin-angiotensin aldosterone system, have been demonstrated in women with superimposed preeclampsia but perform only modestly in its prediction. In addition, central to the pathogenesis of preeclampsia is a tendency toward an antiangiogenic state thought to be triggered by an impaired placenta and, ultimately, contributing to the endothelial dysfunction pathognomonic of the disease. In the general obstetrical population, angiogenic factors, such as soluble fms-like tyrosine kinase-1 and placental growth factor, have shown promise in the prediction of preeclampsia. However, soluble fms-like tyrosine kinase-1 and placental growth factor are impaired in women with chronic hypertension irrespective of whether they develop superimposed preeclampsia. Therefore, the differences in levels are less discriminatory in the prediction of superimposed preeclampsia compared with the general obstetrical population. Alternative biomarkers to the angiogenic and renal factors include those of endothelial dysfunction. A characteristic of both preeclampsia and chronic hypertension is an exaggerated systemic inflammatory response causing or augmenting endothelial dysfunction. Thus, proinflammatory mediators, such as tumor necrosis factor-α, interleukin-6, cell adhesion molecules, and endothelin, have been investigated for their role in the screening and diagnosis of superimposed preeclampsia in women with chronic hypertension. To date, the existing limited evidence suggests that the differences between those who develop superimposed preeclampsia and those who do not are, as with angiogenic factors, also modest and not clinically useful for the stratification of women with chronic hypertension. Finally, pro-B-type natriuretic peptide is regarded as a sensitive marker of early cardiac dysfunction that, in women with chronic hypertension, may predate the pregnancy. Thus, it has been proposed that pro-B-type natriuretic peptide could give insight as to the ability of women with chronic hypertension to adapt to the hemodynamic requirements of pregnancy and, subsequently, their risk of developing superimposed preeclampsia. Although higher levels of pro-B-type natriuretic peptide have been demonstrated in women with superimposed preeclampsia compared with those without, current evidence suggests that pro-B-type natriuretic peptide is not a predictor for the disease. The objectives of this review are to, first, discuss the current criteria for the diagnosis of superimposed preeclampsia and, second, to summarize the evidence for these potential biomarkers that may assist in the diagnosis of superimposed preeclampsia. [ABSTRACT FROM AUTHOR]

Serum fibroblast growth factor 23 (FGF23) levels and the renin-angiotensin-aldosterone system (RAAS) are elevated in chronic kidney disease (CKD) patients, and their association with left ventricular hypertrophy (LVH) has been reported. However, whether the FGF23 elevation is the cause or result of LVH remains unclear. At 10 weeks, male C57BL/6J mice were divided into 4 groups: sham, CKD (5/6 nephrectomy), LVH (transaortic constriction), and CKD/LVH group. At 16 weeks, the mice were euthanized, and blood and urine, cardiac expressions of FGF23 and RAAS-related factors, and cardiac histological analyses were performed. Heart weight, serum FGF23 levels, and cardiac expression of FGF23 and RAAS-related factors, except for angiotensin-converting enzyme 2, were more increased in the CKD/LVH group compared to the other groups. A significant correlation between LVH and cardiac expressions of FGF23 and RAAS-related factors was observed. Furthermore, there was a significantly close correlation of the cardiac expression of FGF23 with LVH and RAAS-related factors. The coexisting CKD and LVH increased serum and cardiac FGF23 and RAAS-related factors, and there was a significant correlation between them. A close correlation of cardiac, but not serum FGF23, with LVH and RAAS suggests that local FGF23 levels may be associated with LVH and RAAS activation. [ABSTRACT FROM AUTHOR]

This study aimed to observe the efficacy and safety of canagliflozin in the treatment of patients with early diabetic nephropathy (DN) and investigate its effect in reducing urinary protein levels. A total of 132 patients with DN and normal renal function (estimated glomerular filtration rate >60 ml/min/1.73 m²) combined with urine albumin/creatinine ratio (UACR) no less than 30 mg/g were selected and randomly divided into a control group and an observation group, with 66 cases in each group. Irbesartan treatment was administered to the control group based on conventional treatment, while a combination of canagliflozin and irbesartan was given to the observation group based on conventional treatment. The changes in blood glucose, blood pressure, body weight, renal function, and urinary protein were observed in both groups. Compared with the control group, patients in the observation group showed a significant decrease in blood glucose, blood pressure, body weight, and urinary protein starting at week 4 of treatment and continuing until the end of the experiment at week 24 (all P<0.05). Within the observation group, blood glucose, blood pressure, body weight, and urinary protein decreased significantly with 24 weeks of treatment compared with those before the experiment (P<0.01). Patients in the observation group experienced a mild decrease in renal function at week 4, but the function began to gradually recover by week 8 and had returned to the baseline by the end of the study (P<0.05). In conclusion: canagliflozin has good efficacy and safety in the treatment of early DN. It also lowers urinary protein levels and blood glucose. [ABSTRACT FROM AUTHOR]

Background: The impact of changes in portal pressure before and after liver resection (defined as ΔHVPG) on postoperative kidney function remains unknown. Therefore, we investigated the effect of ΔHVPG on (i) the incidence of postoperative AKI and (ii) the renin-angiotensin system (RAAS) and sympathetic nervous system (SNS) activity. Methods: We included 30 patients undergoing partial liver resection. Our primary outcome was postoperative AKI according to KDIGO criteria. For our secondary outcome we assessed the plasma renin, aldosterone, noradrenaline, adrenaline, dopamine and vasopressin concentrations prior and 2 h after induction of anaesthesia, on the first and fifth postoperative day. HVPG was measured prior and immediately after liver resection. Results: ΔHVPG could be measured in 21 patients with 12 patients HVPG showing increases in HVPG (∆HVPG≥1 mmHg) while 9 patients remained stable. AKI developed in 7/12 of patients with increasing HVPG, but only in 2/9 of patients with stable ΔHVPG (p = 0.302). Noradrenalin levels were significantly higher in patients with increasing ΔHVPG than in patients with stable ΔHVPG. (p = 0.009). Biomarkers reflecting RAAS and SNS activity remained similar in patients with increasing vs. stable ΔHVPG. Conclusions: Patients with increased HVPG had higher postoperative creatinine concentrations, however, the incidence of AKI was similar between patients with increased versus stable HVPG. [ABSTRACT FROM AUTHOR]

The Hawthorn and Olive are known from ancient time as phytotherapics with beneficial effect on heart and circulatory system, decreasing or regulating the blood pressure. By HPLC analysis were identified polyphenols with proved effect on angiotensin converting enzyme (ACE), the key compound of blood pressure regulation through renin-angiotensin-aldosterone system. The chlorogenic acid, caffeic acid, luteolin, quercitrin and even hyperosid, have the structural elements to block the active center of ACE. Due by the fact that these compounds are in significant quantities, we can conclude that these phyto- and gemmotherapic extracts's normo- or hypotensive effect is done also by the mechanism of ACE inhibition. [ABSTRACT FROM AUTHOR]

This study was conducted to explore the effect of renal denervation (RDN) on the renin–angiotensin–aldosterone system (RAAS) in spontaneously hypertensive rats (SHRs). Our experimental rats were randomly divided into the RDN group conducted by painting 10% phenol on the bilateral renal nerves (RDNX), the shamoperation group simply painting with saline (Sham), and the normotension control group (WKY) following all the animal blood and tissues of kidney, hypothalamus, and adrenal gland collected and examined 2 weeks after RDN operation. We found that the aldosterone (ALD) levels in serum and tissues all decreased in the RDNX group compared with the Sham group (p <.05). Meantime, the expression of angiotensin II type1 receptor (AT1R) mRNA also exhibited significantly reduced by 2.22-fold in the RDNX group compared to the Sham group identical to the expression of AT1R protein in the renal cortex and outer stripe of the outer medulla (OSOM) subjected to denervation surgery, which manifested the lower ATIR protein expression than the Sham group (p <.05). Besides, the expression of angiotensin II (Ang II) protein in the cortex , OSOM, and inner stripe of the outer medulla were all attenuated by RDN in comparison with the Sham group (p <.05). RDN reduced intrarenal RAAS and circulating RAAS to lower blood pressure and repair renal function. [ABSTRACT FROM AUTHOR]

Background: This study investigated the association of angiotensin–converting enzyme (ACE I/D) and aldosterone synthase (CYP11B2-344C/T) gene polymorphisms in the renin–angiotensin–aldosterone system (RAAS) with atrial fibrillation (AF) in the Tunisian population. Materials and Methods: The study population included 120 patients with AF and 123 age-matched controls. Genotyping of the I/D polymorphism in the ACE gene and the -344C/T polymorphism in the CYP11B2 gene was performed by polymerase chain reaction (PCR) and PCR-RFLP methods, respectively. Results: The genotype distribution of the ACE I/D and CYP11B2-344C/T polymorphisms was significantly different between AF patients and control participants (p < 0.01 and p < 0.006 respectively). In addition, ACE I/D increased the risk of AF significantly by 3.41-fold for the DD genotype (OR = 3.41; 95% CI [1.39–8.34]; p < 0.007), and after adjusting for confounding factors (age, diabetes, hypertension, and dyslipidemia), the risk was higher (OR = 5.71; 95% CI [1.48–21.98]; p < 0.01). Likewise, the CYP11B2-344C/T polymorphism increased the incidence of AF for the TT genotype (OR = 3.66; 95% CI [1.62–8.27]; p < 0.002) and the CT genotype (OR = 2.68; 95% CI [1.22–5.86]; p < 0.01). After adjusting for confounding factors (age, diabetes, hypertension and dyslipidemia), the risk remained higher for the TT genotype (OR = 3.58; 95% CI [1.08–11.77]; p < 0.03). Furthermore, the haplotype–based association of the ACE I/D and CYP11B2-344C/T polymorphisms showed that the D-T haplotype increased the risk for AF. Conclusion: Our study suggests a significant association of the ACE (I/D) and CYP11B2-344C/T polymorphisms with AF in the Tunisian population. [ABSTRACT FROM AUTHOR]

Subclinical myocardial dysfunction is prevalent among well-treated persons with HIV (PWH). We have previously demonstrated unique renin-angiotensin-aldosterone system physiology among PWH with metabolic dysregulation. Mineralocorticoid receptor blockade may be a targeted treatment strategy for subclinical heart disease in PWH. Forty-six PWH were randomized to receive either eplerenone 50 mg daily or placebo in a 6-month randomized, double-blinded, placebo-controlled trial. We assessed changes in N-terminal pro-B-type natriuretic peptide (NT-proBNP), a biomarker of cardiac stretch, under controlled posture and dietary conditions. The eplerenone- and placebo-treated groups demonstrated a long duration of HIV with good immunological control. NT-proBNP levels were similar between the groups at baseline (41.1 [20.2, 97.9] vs 48.9 [29.2, 65.4] ng/L, P =.80) and decreased significantly more in the eplerenone- vs placebo-treated groups after 6 months (change NT-proBNP -9.6 [-46.8, 0.3] vs -3.0 [-17.0, 39.9] ng/L, P =.02 for comparison of change between groups). Decreases in NT-proBNP were independent of changes in systolic and diastolic blood pressure, and related to decreases in high-sensitivity C-reactive protein (ρ = 0.32, P =.05) and inversely to increases in serum aldosterone (ρ = -0.33, P =.04) among all participants. Treatment with eplerenone for 6 months vs placebo significantly decreases NT-proBNP levels among PWH, independent of eplerenone's known blood pressure-lowering effects. Further studies should elucidate whether lowering NT-proBNP in this at-risk metabolic population with subclinical heart disease will offer cardioprotection. Clinical Trial Registration NCT01405456 [ABSTRACT FROM AUTHOR]

Until recently, most studies of heart failure (HF) focused on body fluid dynamics through control of the sodium and water balance in the body. Chloride has remained largely ignored in the medical literature, and in clinical practice, chloride is generally considered as an afterthought to the better-known electrolytes of sodium and potassium. In recent years, however, the important role of chloride in the distribution of body fluid has emerged in the field of HF pathophysiology. Investigation of HF pathophysiology according to the dynamics of serum chloride is rational considering that chloride is an established key electrolyte for tubulo-glomerular feedback in the kidney and a possible regulatory electrolyte for body fluid distribution. The present review provides a historical overview of HF pathophysiology, followed by descriptions of the recent attention to the electrolyte chloride in the cardiovascular field, the known role of chloride in the human body, and recent new findings regarding the role of chloride leading to the proposed 'chloride theory' hypothesis in HF pathophysiology. Next, vascular and organ congestion in HF is discussed, and finally, a new classification and potential therapeutic strategy are proposed according to the 'chloride theory'. [ABSTRACT FROM AUTHOR]

The landscape of HIV medicine dramatically changed with the advent of contemporary antiretroviral therapies, which has allowed persons with HIV (PWH) to achieve good virologic control, essentially eliminating HIV-related complications and increasing life expectancy. As PWH are living longer, noncommunicable diseases, such as cardiovascular disease (CVD), have become a leading cause of morbidity and mortality in PWH with rates that are 50% to 100% higher than in well-matched persons without HIV. In this review, we focus on disease of the coronary microvasculature and myocardium in HIV. We highlight a key hormonal system important to cardiovascular endocrinology, the renin-angiotensin-aldosterone system (RAAS), as a potential mediator of inflammatory driven-vascular and myocardial injury and consider RAAS blockade as a physiologically targeted strategy to reduce CVD in HIV. [ABSTRACT FROM AUTHOR]

A review of current publications suggests that patients with arterial hypertension (AH) are at increased risk for severe course and fatal outcome of COVID-19. The main pathogenetic mechanisms explaining the association of AH with COVID-19 include the effect of coronavirus on the functioning of the renin-angiotensin-aldosterone system (RAAS), which is involved in the development and progression of AH. The review presents the results of a number of studies evaluating the effect of the use of ACE inhibitors / ARBs on the development and course of COVID-19 in patients with cardiovascular diseases. The results of international data analysis showed that the use of ACE inhibitors / ARBs in patients with AH and COVID-19 is associated with lower rates of total mortality, and the use of ACE inhibitors, statins and the female sex are associated with a greater likelihood of patient survival. The data on the promising development of new drugs affecting the functioning of RAAS are presented.

Abstract Background Plasma aldosterone-to-renin ratio (ARR) is popularly used for screening primary aldosteronism (PA). Some medications, including diuretics, are known to have an effect on ARR and cause false-negative and false-positive results in PA screening. Currently, there are no studies on the effects of sodium–glucose cotransporter-2 (SGLT2) inhibitors, which are known to have diuretic effects, on ARR. We aimed to investigate the effects of SGLT2 inhibitors on ARR. Methods We employed a retrospective design; the study was conducted from April 2016 to December 2018 and carried out in three hospitals. Forty patients with diabetes and hypertension were administered SGLT2 inhibitors. ARR was evaluated before 2 to 6 months after the administration of SGLT2 inhibitors to determine their effects on ARR. Results No significant changes in the levels of ARR (90.9 ± 51.6 vs. 81.4 ± 62.9) were found. Body mass index, diastolic blood pressure, heart rate, fasting plasma glucose, and hemoglobin A1c were significantly decreased by SGLT2 inhibitors. Serum creatinine was significantly increased. Conclusion SGLT2 inhibitor administration yielded minimal effects on ARR and did not increase false-negative results in PA screening in patients with diabetes and hypertension more than 2 months after administration.

Aim.To study an activity of the Renin-Angiotensin-Aldosterone System (RAAS) components in patients with primary hyperparathyroidism (PHPT) before and after parathyroidectomy (PTE). Materials and methods.A comparative study of patients with PHPT and control group. The first stage of the study included 56 patients with PHPT (group 1) before and on the third day after PTE. The second stage was carried out in 27 patients with remission of PHPT (group 2). All patients and healthy volunteers were tested for the main parameters of phosphorus-calcium metabolism and the RAAS parameters (plasma renin activity PRA, serum aldosterone, angiotensin II AT II). Results.Patients with active PHPT demonstrated changes in RAAS activity (lower PRA, higher AT II level) comparing to control group, that have statistical significance in group 1 (p0.001 for both parameters). There were no significant differences in aldosterone levels (p1=0.090;p2=0.140). On the third day after PTE (group 1), a decrease in aldosterone level (p=0.009) and a tendency to decrease in PRA (p=0.030) were detected. However, an increase in PRA (p=0.018), a decrease in AT II concentration (p=0.032) comparing to the initial values and their normalization were observed 12 months after surgery when permanent normal serum calcium and PTH levels had been achieved. There were controversial correlations between the parameters of phosphorus-calcium metabolism and RAAS. The influence of angiotensin-converting-enzyme inhibitors and AT II receptor blockers on phosphorus-calcium metabolism in patients with PHPT was not observed. Conclusion.In patients with PHPT, there were no сlear correlations of phosphorus-calcium metabolism parameters with RAAS, however an increase of AT II concentration was noted, that can take part in a development of hypertension for this endocrinopathy. PTE can have a positive effect on AT II level.

In the pathogenesis of arterial hypertension (AH), the renin-angiotensin-aldosterone system plays a key role in helping to maintain elevated blood pressure. At the same time, the state of angiotensin-II production (AT II) and the expression level of its receptors on target cells determine the formation of most of the effects underlying the pathogenesis of associated clinical conditions in such patients. Thus, the study of the pathogenesis of AH, namely the study of the role of the AT II axis, the AT II receptor, is an actual scientific and practical task. Aim. Given the important role of type 1 receptors for AT II in the formation of pathological changes in arterial hypertension, the purpose of this study was to study the peculiarities of the effect of their expression on biochemical processes in patients with arterial hypertension. Material and methods. In the course of the clinical study, 60 patients of both sexes with hypertension aged 45 to 55 years old were admitted to the clinic for planned treatment. Depending on the initial level of expression of receptors for AT II (AT1R), determined by the serum concentration of the soluble form of type 1 receptors for AT II, the patients were divided into two subgroups with conditionally low (corresponding to the concentration of the soluble form of the receptor for AT II 0.66 ng/ml) and conditionally high (1.57 ng/ml) expression. The analysis showed that high expression of AT1R is associated with elevated plasma levels of renin by 30.8% (p=0.0005), AT II by 48.1% (p=0.00001), E-selectin by 47.9% (p=0.0001), VCAM-1 by 29.1% (p=0.00001), ICAM-1 by 52.9% (p=0.00001), VE-cadherin by 50.9% (p=0.00001), endothelin-1 by 48.8% (p=0.0005), an ACE inhibitor by 13.6% (p=0.047), and CRP by 74.1% (p=0.00002 ) and endoperoxide by 29.7% (p=0.009). Against this background, there was a decrease in the level of apoA1 by 21.6% (p=0.027), ACE by 20.1% (p=0.1), the level of antioxidants by 22.3% (p=0.00001). The analysis showed that in the group with initially high expression of AT1R, there was an increased blood pressure, the level of which, on average, exceeded the values of patients with low expression of the indicated receptor by 24.5 mm Hg (p=0.011). Against the background of therapy in the group with high expression of AT1R, plasma renin activity decreased by 20.3% (p=0.013), endoperoxide by 8.4% (p=0.038), an ACE inhibitor by 14.6% (p=0.02). At the same time, the level of apoA1 increased by 8.5% (p=0.036), antioxidants by 8.6% (p=0.036), ICAM-1 by 5.3% (p=0.05), VE-cadherin by 2.5% (p=0.07). The level of the remaining factors was not statistically significant. In the subgroup with low expression of the AT II receptor, during treatment, there was a decrease in endoperoxide by 12.8% (p=0.031), an ACE inhibitor by 5.5% (p=0.044) without significant changes in other indicators. Conclusion. In hypertensive patients, higher expression of AT1R is associated with high activation of immune-inflammatory mechanisms, dyslipidemia, an imbalance of the lipid peroxidation system and antioxidant protection, as well as higher renin-angiotensin-aldosterone system activity and increased arterial pressure. On the background of antihypertensive therapy, partial compensation of the identified changes is achieved, including a moderate increase in the level of antioxidants, a decrease in the concentration of endoperoxide, renin activity and an increase in the level of apoA1, while maintaining an increased level of AT II, high expression of receptors to it. These changes indicate the need for further search for effective antihypertensive therapy strategies aimed at limiting the activity of renin-angiotensin-aldosterone system in patients with hypertension.

Accumulating evidence suggests that obesity is a major risk factor for the initiation, progression, and outcomes of coronavirus disease 2019 (COVID-19). The European Association for the Study of Obesity (EASO), as a scientific and medical society dedicated to the promotion of health and well-being, is greatly concerned about the concomitant obesity and COVID-19 pandemics and their impact on health and society at large. In this perspective, we will address the inherent immunological perturbations and alterations in the renin-angiotensin-aldosterone system in patients with obesity and COVID-19, and discuss how these impairments may underlie the increased susceptibility and more detrimental outcomes of COVID-19 in people with obesity. Clearly, this has important implications for preventive measures, vaccination, and future therapeutic strategies to combat COVID-19. Furthermore, we will highlight important knowledge gaps and provide suggestions for future research and recommendations for policy actions. Since many new reports on COVID-19 rapidly appear, the present perspective should be seen as a focus for discussion to drive forward further understanding, research initiatives, and clinical management of COVID-19.

Objectives to study the indicators of humoral regulation of circulatory system in obese patients as the predictors of CHF development. Materials and methods.Two groups of 40 patients were formed: the first group consisted of patients with I or II grades obesity with BMI of up to 40 kg/m2, the second group included patients with grade III obesity with BMI of over 40 kg/m2. None of the selected patients had a history of cardiovascular events. The concentration value of renin-angiotensin-aldosterone system components and level of N-terminal pro B-type natriuretic peptide (NT-pro-BNP) was determined. Results.Aldosterone level in grade III obese patients was close to normal upper border: 58.9 [54.9; 73.8] pg/ml (normal range is 1060 pg/ml), while in patients with grade III obesity it was 79.5 [64.5; 90.1], which is 25.9% higher than in patients of the first group and 24.5% higher above the normal level (p 0.05). These two groups was significantly different not only in average plasma aldosterone level, but in absolute number of patients with hyperaldosteronism, whose number accounted for 46.2% in grades I or II obese patients and 85.7% among patients with grade III obesity. Plasma renin level and angiotensin II levels in both groups was within the normal range. NT-proBNP level in the first group was 23.7 [10.6; 23.6] pg/ml, in the second group 138.0 [121.5; 145.9] pg/ml, which is 5.8 times higher (p = 0.001). In both groups of patients, the correlation analysis showed that aldosterone and NT-proBNP levels are closely related (r = 0.74, p 0.05). Conclusion.This study suggests that aldosterone level can be used as a predictor of HF.

Abstract Aims The angiotensin receptor neprilysin inhibitor (ARNI) sacubitril/valsartan reduces mortality and hospitalizations in patients with heart failure and reduced ejection fraction (HFrEF). Favourable effects on haemodynamic and functional parameters have been observed in patients with HFrEF undergoing ARNI therapy, using standard transthoracic echocardiography. Global longitudinal strain (GLS) assessment uses a semi‐automatic procedure to provide a reliable and repeatable method that improves the detection of early changes of contractile function. We aimed to assess the effects of ARNI on GLS and myocardial mechanics in patients with HFrEF. Methods and results Thirty patients with New York Heart Association class II–III HFrEF were treated with ARNI and monitored using standard echocardiographic examination and GLS measurements at baseline, 3 months, and 6 months. ARNI therapy resulted in a significant reduction of ventricular volumes and a significant increase in left ventricular ejection fraction at 6 months but not 3 months by standard transthoracic echocardiography (left ventricular ejection fraction from 28 ± 8% at baseline to 34 ± 12% at 6 months, P

Abstract Background To investigate the relationships of plasma renin, angiotensin, and aldosterone levels to blood pressure variability and target organ damage in children with essential hypertension. Methods A case-control study was conducted on 132 children diagnosed with essential hypertension (103 males and 29 females with the mean age of 11.8 ± 2.4 years). The plasma RAAS levels were measured using the enhanced chemiluminescence method, the ambulatory blood pressure was monitored for 24 h, and then the average real variability (ARV) was calculated. Data on indicators were used for assessing cardiac and renal damages. The correlations of plasma renin, angiotensin, and aldosterone (RAAS) levels to blood pressure variability (BPV) and target organ damage (TOD) were studied. A comparison between the groups was conducted using SPSS 20. Results Among the 132 children, 55 cases had target organ damage. The 24-h ARV and the daytime ARV of the systolic blood pressure of the high angiotensin II (AT II) group was significantly higher than that of the normal AT II group (t = 2.175, P = 0.031; t = 2.672, P = 0.009). Plasma AT II and aldosterone levels were significantly associated with the left ventricular mass index (r = 0.329, P = 0.0001; r = 0.175, P = 0.045). Linear regression analysis showed that AT II [β ± s.e. = 0.025 ± 0.006, 95% CI (0.013–0.038), P = 0.0001] and aldosterone [β ± s.e. = 0.021 ± 0.007, 95% CI (0.008–0.034), P = 0.002] were risk factors for LVH. Conclusions The AT II level in children with essential hypertension affected the variability of the 24-h and the daytime SBP. Plasma AT II and aldosterone levels were associated with cardiac damage. Results from this study indicated that AT II and aldosterone are risk factors for LVH in childhood hypertension and are of great significance for improving the clinical prognosis of pediatric patients with hypertension.

Angiotensin-converting enzyme 2 (ACE2) is the receptor for SARS-CoV and SARS-CoV-2(severe acute respiratory syndrom coronavirus 2) viruses, and it is also one of the main family members of renin-angiotensin-aldosterone system. ACE2 has a protective effect on cardiovascular diseases and inhibits the development of cardiovascular diseases. SARS-CoV-2 reduces the expression of ACE2 of host, which may be one of the reasons for cardiovascular complications in the later stage of coronavirus disease 2019(COVID-19). Thus, the role and mechanism of ACE2 in the development of cardiovascular diseases were summarized in this article in order to provide potential stratigy development for the treatment of COVID-19.

Abstract Background Overactivation of renin-aldosterone-angiotensin system (RAS) is part of the pathogenesis of obesity-associated hypertension. Evidences have shown that weight loss can result in reduction in blood pressure and RAS. This study was aim to investigate changes of plasma aldosterone concentration (PAC) after bariatric surgery. Methods A prospective study was done in 14 morbidly obese patients undergoing bariatric surgery. Patients who were taking medications that can interfere with PAC and renin levels were excluded. Collection of blood samples were done at baseline and at 3 and 6-month post-bariatric surgery. Results Four out of 14 patients had hypertension at baseline. Mean body mass index (BMI) was 56.7 ± 13.5 kg/m2. PAC were significantly decreased at 3-and 6-month post-bariatric surgery from 14.3 ± 8.0 to 7.5 ± 5.5 [reduction of 36% from baseline (P