Journal of the Renin-Angiotensin-Aldosterone System最新文献

{"title":"Haplotype-based association study between PRCP gene polymorphisms and essential hypertension in Hani minority group from a remote region of China.","authors":"Yanrui Wu,&nbsp;Xingming Pan,&nbsp;Xiaoxiao Jin","doi":"10.1177/1470320320981316","DOIUrl":"https://doi.org/10.1177/1470320320981316","url":null,"abstract":"<p><strong>Objective: </strong>Prolylcarboxypeptidase (PRCP) is both involved in the Kallikrein-Kinin system (KKS) and renin-angiotensin-aldosterone system (RAAS). This study aimed to determine the genetic impact of PRCP gene polymorphisms on essential hypertension (EH) in an isolated population from a remote region of China.</p><p><strong>Methods: </strong>A haplotype-based study was investigated in 346 EH patients and 346 normal subjects and all samples were Hani minority residents in Southwest China. A total of 11 tag single nucleotide polymorphisms (SNPs) in PRCP gene were tested by polymerase chain reaction-restriction fragment length polymorphism method.</p><p><strong>Results: </strong>Single site analysis found that PRCP gene 3'UTR SNP rs3750931 was associated with EH. The minor allele G of rs3750931 was more prevalent in the EH patients compared to control subjects after Bonferroni correction (<i>p</i> < 0.05). Moreover, the rs3750931 G allele carriers showed higher average blood pressure (BP) level among the subjects. The H2 (GAGCACTAACA) haplotype without rs3750931 G allele showed the protective effect for EH (OR = 0.68, 95 CI 0.54-0.85, <i>p</i> = 0.001).</p><p><strong>Conclusion: </strong>The present study indicated PRCP gene rs3750931 was associated with the risk of EH. This SNP G allele could be considered as one of risk markers for EH in Hani population.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320981316","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38710851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The value of the post-captopril aldosterone/renin ratio for the diagnosis of primary aldosteronism and the influential factors: A meta-analysis.","authors":"Qiao Xiang,&nbsp;Wen Wang,&nbsp;Tao Chen,&nbsp;Kai Yu,&nbsp;Qianrui Li,&nbsp;Tingting Zhang,&nbsp;Haoming Tian,&nbsp;Yan Ren","doi":"10.1177/1470320320972032","DOIUrl":"https://doi.org/10.1177/1470320320972032","url":null,"abstract":"<p><strong>Objective: </strong>The procedure for the captopril challenge test (CCT) in diagnosing primary aldosteronism (PA) is not standardized. We performed a meta-analysis to evaluate the controversial diagnostic value and influential factors of the post-captopril aldosterone/renin ratio (ARR).</p><p><strong>Methods: </strong>We searched literature in databases for eligible studies (until October 1, 2020). We extracted information regarding study and patient characteristics, CCT methods, outcome data. We pooled studies using the random-effect model. We performed meta-regression and six pre-specified subgroup analyses to explore heterogeneity.</p><p><strong>Results: </strong>Nineteen studies involving 4568 subjects were included. The pooled sensitivity and specificity were 0.825 (95% CI 0.804-0.844) and 0.919 (95% CI 0.908-0.928). The area under the summary receiver operating characteristic curve was 0.9487 (95% CI 0.9207-0.9767). Meta-regression revealed that heterogeneity might derive from time interval (<i>p</i> = 0.0117) and study population (<i>p</i> = 0.0033). Subgroup analyses showed significant differences between the subgroups stratified by the dose, posture, study region, time interval, cut-off value and study population for sensitivity and/or specificity (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>Post-captopril ARR is comparably valuable for diagnosing PA at cut-offs from 12.0 to 50.0. Conducting the CCT in the supine position with 25 mg of captopril may attain greater sensitivity. Conducting the CCT in the seated position with 50 mg of captopril may attain greater specificity. A 90-min time interval may perform best in both the sensitivity and specificity.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320972032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38641969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Central involvement of SARS-CoV-2 may aggravate ARDS and hypertension.","authors":"Erkan Cure,&nbsp;Medine Cumhur Cure,&nbsp;Hulya Vatansev","doi":"10.1177/1470320320972015","DOIUrl":"https://doi.org/10.1177/1470320320972015","url":null,"abstract":"Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). Dear Sir, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to spread rapidly all over the world; however, the mechanism of the disease is not yet fully understood. Why do many people who come into contact with the virus not get sick and remain asymptomatic? Why do some people recover with tiny symptoms, while other people have a severe infection or die? SARSCoV-2 infection can lead to severe or fatal outcomes in patients with comorbid diseases such as hypertension, diabetes, obesity, and heart failure. SARS-CoV-2 binds to angiotensin-converting enzyme (ACE)-2, like SARS-CoV, enters the cells and causes infection. The renin-angiotensin system (RAS) plays a crucial role in the virus entry to cells and the progression of the virus-induced disease. Whether ACE2 upregulation will increase viral load remains unclear.1 ACE2 up-regulation increases angiotensin 1–7 formation and may have a protective effect against SARSCOV-2 caused acute respiratory distress syndrome (ARDS) and heart damage.1 Angiotensin II level is high in patients with the novel coronavirus disease 2019 (COVID19). According to an extensive view, SARS-CoV-2 binds to ACE2, causing ACE2 to become dysfunctional.2 Therefore, increased angiotensin II level leads to ARDS and heart damage.2 Interestingly, most infected people have no symptoms, and they do not have heart or lung damage. The effects of SARS-CoV-2 on peripheral RAS have been highlighted so far. We believe that the central RAS involvement of the virus has vital implications for COVID-19 progression. Regulation of pulmonary vascular tone is vital for the maintenance of pulmonary functions. RAS regulates vasoconstriction and vasodilation of the pulmonary vascular system. Bradykinin and kinin are responsible for the permeability and vasodilation of the pulmonary vascular system (Figure 1). Inflammation leads to an increase in bradykinin-1 receptor (B1R) in the lungs. They increase vascular permeability by binding bradykinin to the bradykinin-2 receptor (B2R) and des-arg9-bradykinin binding to the B1R. Increased pulmonary vascular permeability causes pulmonary edema.3,4 SARS-CoV-2 can cause ARDS via the bradykinin pathway in the lung (Figure 1).3,4 The brain is one of the tissues containing ACE2, such as the lung, heart, pancreas, kidney, and vascular endothelium, and SARS-CoV-2 can easily infect the brain.5,6 The virus infects the brain after can cross the blood-brain barrier either by direct transport through the bloodstream or indirectly by binding to the vascular endotheliu","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320972015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38592575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Countermeasure and therapeutic: A(1-7) to treat acute respiratory distress syndrome due to COVID-19 infection.","authors":"Maira Soto,&nbsp;Gere diZerega,&nbsp;Kathleen E Rodgers","doi":"10.1177/1470320320972018","DOIUrl":"https://doi.org/10.1177/1470320320972018","url":null,"abstract":"<p><p>In the wake of the COVID-19 pandemic it has become clear that there is a need for therapies that are capable of reducing damage caused to patients from infections. Infections that induce Acute Respiratory Distress Syndrome (ARDS) are especially devastating because lung damage is so critical and difficult to manage. Angiotensin (1-7) [A(1-7)] has already been shown to protect pulmonary health and architecture in various models of disease. There is also evidence that A(1-7) can modulate immune function and protect various organs (lung, kidney, and heart) from oxidative damage and inflammation. Here we focus on making a case for the development of novel therapies that target the protective arm of the Renin Angiotensin System (RAS).</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320972018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38689219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of contrast-induced acute kidney injury on the association between renin-angiotensin system inhibitors and long-term mortality in heart failure patients.","authors":"Li Lei,&nbsp;Yulu Huang,&nbsp;Zhaodong Guo,&nbsp;Feier Song,&nbsp;Yibo He,&nbsp;Jin Liu,&nbsp;Guoli Sun,&nbsp;Bowen Liu,&nbsp;Pengyuan Chen,&nbsp;Jianbin Zhao,&nbsp;Dengxuan Wu,&nbsp;Yan Xue,&nbsp;Wenhe Yan,&nbsp;Zefeng Lin,&nbsp;Xiuqiong Huang,&nbsp;Guanzhong Chen,&nbsp;Shiqun Chen,&nbsp;Yong Liu,&nbsp;Jiyan Chen","doi":"10.1177/1470320320979795","DOIUrl":"https://doi.org/10.1177/1470320320979795","url":null,"abstract":"<p><strong>Introduction: </strong>Renin-angiotensin system inhibitors (RASi) reduce mortality among heart failure (HF) patients, but their effect among those complicating contrast-induced acute kidney injury (CI-AKI) remains unexplored. We aimed to investigate whether the relationship between RASi prescription at discharge and mortality differs between HF patients with or without CI-AKI following coronary angiography (CAG).</p><p><strong>Methods: </strong>About 596 HF patients from an observational cohort were divided into a CI-AKI group (<i>n</i> = 104) and a non-CI-AKI group (<i>n</i> = 492) based on whether they had CI-AKI following CAG. The endpoint was all-cause mortality. Multivariable Cox regression was performed in each group to explore the associations between RASi at discharge and mortality.</p><p><strong>Results: </strong>During the median follow-up time of 2.26 (1.70; 3.24) years, higher mortality rate was observed in the CI-AKI group compared to the non-CI-AKI group (18.3% vs 8.9%, <i>p</i> = 0.002). Among HF patients with CI-AKI, after adjusting for confounding factors, the association was not significant between RASi prescription at discharge and mortality (HR: 0.39, 95%CI: 0.12-1.31, <i>p</i> = 0.128), while it was among those without CI-AKI (HR: 0.39, 95%CI: 0.18-0.84, <i>p</i> = 0.016).</p><p><strong>Conclusion: </strong>RASi prescription at discharge for HF patients complicating CI-AKI tended to be ineffective, while it benefited those without CI-AKI. Further randomized evidence is needed to confirm this trend.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320979795","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38373375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin-converting enzyme 2, the complement system, the kallikrein-kinin system, type-2 diabetes, interleukin-6, and their interactions regarding the complex COVID-19 pathophysiological crossroads.","authors":"Martijn Hoevenaar, Dolf Goossens, Janne Roorda","doi":"10.1177/1470320320979097","DOIUrl":"10.1177/1470320320979097","url":null,"abstract":"<p><p>Because of the current COVID-19-pandemic, the world is currently being held hostage in various lockdowns. ACE2 facilitates SARS-CoV-2 cell-entry, and is at the very center of several pathophysiological pathways regarding the RAAS, CS, KKS, T2DM, and IL-6. Their interactions with severe COVID-19 complications (e.g. ARDS and thrombosis), and potential therapeutic targets for pharmacological intervention, will be reviewed.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320979097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38343724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The genetic polymorphisms of angiotensin converting enzyme insertion/deletion and glioma susceptibility: A meta-analysis.","authors":"Meili Sun,&nbsp;Yuying Fang,&nbsp;Shuzhen Ma,&nbsp;Ximei Gao,&nbsp;Yuping Sun","doi":"10.1177/1470320320963939","DOIUrl":"https://doi.org/10.1177/1470320320963939","url":null,"abstract":"<p><strong>Objective: </strong>The previous studies on angiotensin converting enzyme (ACE) insertion/deletion (I/D) genetic polymorphism and glioma risk were inconsistent. Therefore, we performed a meta-analysis to assess the association between ACE I/D polymorphisms and glioma risk.</p><p><strong>Methods and results: </strong>In total, four populations (1110 cases and 1335 controls) on ACE I/D polymorphism were included. Overall, the meta-analysis demonstrated no significant association between ACE I/D polymorphism and glioma risk. In addition, the analysis of the association of ACE I/D polymorphism and clinical grade also showed no significant association.</p><p><strong>Conclusion: </strong>Our meta-analysis didn't find a significant association between ACE I/D polymorphism glioma risk. However, further studies with larger sample size and more ethnic groups are required to confirm the results.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320963939","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38478908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensinogen M235T polymorphism and susceptibility to hypertrophic cardiomyopathy in Asian population: A meta analysis.","authors":"Zhen Zhen, Lu Gao, Qin Wang, Xi Chen, Jia Na, Xiwei Xu, Yue Yuan","doi":"10.1177/1470320320978100","DOIUrl":"10.1177/1470320320978100","url":null,"abstract":"<p><strong>Objective: </strong>To explore the relationship between the polymorphism of angiotensinogen gene (AGT) M235T and susceptibility to hypertrophic cardiomyopathy (HCM) in Asian population by meta-analysis.</p><p><strong>Methods: </strong>PubMed, Embase, Web of Science, Cochrane library, CNKI, Wan Fang, and other databases were searched to collect the literature about AGT M235T polymorphism and HCM from the inception to March 1, 2020. The Newcastle-Ottawa Scale (NOS) checklist was uesd to perform independent literature review and study quality assessment. Data was analyzed by Stata 15.0 software.</p><p><strong>Results: </strong>The results showed that, except for the recessive genetic model (TT vs MT+MM: OR = 1.27, 95%CI: 1.05-1.53), in the other four genetic models, the M235T polymorphism had no significant correlation with the risk of HCM (T vs M: OR = 1.17, 95%CI: 0.88-1.57; TT+MT vs MM: OR = 1.13, 95%CI: 0.55-2.33; TT vs MM: OR = 1.25, 95%CI: 0.60-2.59; TM vs MM: OR = 0.95, 95%CI0.5-1.82). The results of subgroup analysis showed that, except for the heterozygous genetic model, in the other four genetic models, M235T polymorphism was significantly associated with sporadic hypertrophic cardiomyopathy (SHCM), but not with familial hypertrophic cardiomyopathy (FHCM) (<i>p</i> > 0.05).</p><p><strong>Conclusion: </strong>M235T polymorphism in Asians is associated with HCM, especially SHCM. Heterozygotes increase the risk of patients with SHCM.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5b/43/10.1177_1470320320978100.PMC7734517.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38696739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COVID-19 and the pulmonary vascular injury.","authors":"Hai-Long Dai,&nbsp;Xue-Feng Guang","doi":"10.1177/1470320320972276","DOIUrl":"https://doi.org/10.1177/1470320320972276","url":null,"abstract":"Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). Dear Sir, Since December 2019, an outbreak of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in Wuhan, which imposes significant threats to global public health. Studies found that SARS-CoV-2 and SARS-Cov share the same receptor, angiotensin-converting enzyme 2 (ACE2),1,2 SARS-CoV-2 have a 10to 20-fold higher affinity for ACE2 than SARS-CoV,3 and the pathogenic mechanism may be shared between these two viruses.4 The renin–angiotensin system (RAS) plays important role in cardiovascular system. ACE2, a homolog of ACE, is a carboxypeptidase that degrades angiotensin (Ang) II to Ang-(1–7). ACE2 plays an important role in the vasodilative axis (ACE2–Ang-(1–7)–Mas axis) of the RAS and counterbalances the vasoconstrictive, proliferative, and fibrotic axes (ACE–Ang II–Ang II type 1 receptor (AT1R) axis) of the RAS.5 ACE2 is highly expressed in the lungs and heart. Since then, an abundance of evidence has supported the fundamental concept that ACE2 is protective against a variety of cardiopulmonary vascular diseases, including heart failure, hypertension, pulmonary arterial hypertension (PAH).6–8 In the lungs, activation of local pulmonary RAS can affect the pathogenesis of lung injury, high levels of Ang II can lead to increases in vascular permeability and alterations of alveolar epithelial cells.9 In SARS-CoV infection of mice, both viral replication and the viral spike protein alone have been shown to selectively reduce ACE2.10 SARS-CoV also induces rapid downregulation of ACE2 from the cell surface.11 The entry of SARS-CoV2 into the cells through membrane fusion also markedly down-regulates ACE2 receptors.12 Balancing ACE/ACE2 axis may be alleviate virus-induced severe lung injury. ACE Inhibitors (ACEIs) and Angiotensin Receptor Blockers (ARBs) may help reduce lung injury caused by viral infection.13,14 So, for SARS-CoV-2 infected patients with hypertension, ACEIs and ARBs may be a good choice.15–17 ACE2 is also expressed in endothelial cells, especially lung microvascular endothelial cell.18–20 The decrease of ACE2 is related to pulmonary vascular remodeling and PAH.21 These results suggest that SARS-CoV-2 infection may cause pulmonary vascular injury and remodeling by disrupted the balance between ACE/ACE2 and Ang II/ Ang-(1–7) (Figure 1). ACE2 has been shown to be decreased in the plasma of patients with PAH, those patients are more likely to develop into severe patients after SARS-CoV-2 infection. So, we suggest that special care of pulmonary vasc","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320972276","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38590080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amiloride: A review.","authors":"Qianhui Sun,&nbsp;Peter Sever","doi":"10.1177/1470320320975893","DOIUrl":"https://doi.org/10.1177/1470320320975893","url":null,"abstract":"<p><p>Amiloride is a potassium retaining diuretic and natriuretic which acts by reversibly blocking luminal epithelial sodium channels (ENaCs) in the late distal tubule and collecting duct. Amiloride is indicated in oedematous states, and for potassium conservation adjunctive to thiazide or loop diuretics for hypertension, congestive heart failure and hepatic cirrhosis with ascites. Historical studies on its use in hypertension were poorly controlled and there is insufficient data on dose-response. It is clearly highly effective in combination with thiazide diuretics where it counteracts the adverse metabolic effects of the thiazides and its use in the Medical Research Council Trial of Older Hypertensive Patients, demonstrated convincing outcome benefits on stroke and coronary events. Recently it has been shown to be as effective as spironolactone in resistant hypertension but there is a real need to establish its potential role in the much larger number of patients with mild to moderate hypertension in whom there is a paucity of information with amiloride particularly across an extended dose range.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320975893","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38637311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}