Hypertension最新文献

{"title":"Perirenal Adipose Tissue and Hypertension: Observational and Genetic Analyses.","authors":"Hang Shen,Zhipeng Wu,Wenjin Luo,Xiangjun Chen,Jun Yang,Qinglian Zeng,Chunxue He,Yun Mao,Linqiang Ma,Rufei Gao,Zhihong Wang,Qifu Li,Shumin Yang,Jinbo Hu","doi":"10.1161/hypertensionaha.125.24995","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.24995","url":null,"abstract":"BACKGROUNDPerirenal adipose tissue (PRAT) consists of white and brown adipocytes with good vascularization and dense innervation, which could influence the blood pressure. We aim to investigate the association of PRAT thickness with risks of overall and specific forms of hypertension.METHODSWe measured PRAT thickness in the UK Biobank and CONPASS (Chongqing Primary Aldosteronism Study). We prospectively examined the correlation between PRAT thickness and incident hypertension in the UK Biobank. We cross-sectionally explored associations between PRAT thickness and common forms of hypertension in CONPASS. Integrating data from GWAS (Genome-Wide Association Study), we investigated the potential causal relationship between PRAT and hypertension forms by 2-sample Mendelian randomization analyses.RESULTSIn the prospective analysis of the UK Biobank, participants whose PRAT thickness was ≥46.1 mm showed a higher risk of developing hypertension than participants whose PRAT thickness was <16.4 mm (hazard ratio, 2.91 [95% CI, 1.97-4.32]). In the cross-sectional analysis of CONPASS, a 1 SD increment in PRAT thickness was associated with a 2.77-fold higher adjusted odds of low-renin essential hypertension and a 3.89-fold higher adjusted odds of idiopathic hyperaldosteronism. PRAT thickness was not significantly associated with other forms of hypertension, such as aldosterone-producing adenoma and obstructive sleep apnea. In 2-sample Mendelian randomization analyses, PRAT thickness was only significantly associated with a higher risk of idiopathic hyperaldosteronism (inverse variance weighted odds ratio, 1.33 [95% CI, 1.09-1.62]), with no evidence of significant heterogeneity or substantial directional pleiotropy.CONCLUSIONSPRAT is causally associated with idiopathic hyperaldosteronism rather than essential hypertension and other forms of secondary hypertension.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"11 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144720171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00599 Promotes Pulmonary Hypertension via Liquid-Liquid Phase Separation With G3BP1 and MYH9.","authors":"Yingqi Wang,Lulu Yin,Shuang Zheng,Aijing Liu,Chunmiao Liu,Zhitu Bao,He Zhu,Xiaoxu Zhao,Ziru Zhao,Yu Pan,Daling Zhu,Hang Yu","doi":"10.1161/hypertensionaha.124.24511","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.24511","url":null,"abstract":"BACKGROUNDPulmonary hypertension (PH) represents a significant cardiovascular disorder marked by both functional and structural alterations within the pulmonary vasculature. Long noncoding RNAs have been closely associated with PH pathogenesis and progression, particularly in vascular remodeling and cell proliferation. Nonetheless, how long noncoding RNAs interact with downstream targets to modulate PH remains unclear.METHODSThe expression levels of LINC00599 were quantified in the mouse lung tissues and pulmonary arterial smooth muscle cells (PASMCs) under hypoxic conditions. The involvement of LINC00599 in PH progression and vascular remodeling was evaluated through in vivo studies. To investigate its role in human PASMC proliferation, small interfering RNA and overexpression plasmids were used.RESULTSThe expression of LINC00599 is upregulated in the medial layer of pulmonary arteries in experimental PH models and hypoxic PASMCs. Administration of lentivirus-mediated shRNA targeting LINC00599 reverses hypoxic PH in murine models. Mechanistically, LINC00599 promotes PASMC proliferation by modulating stress granule formation through m6A (N6-methyladenosine) modification and facilitating liquid-liquid phase separation with MYH9 (myosin heavy chain 9), a process previously implicated in cell-cycle regulation. Furthermore, its expression is driven by a super-enhancer mediated by the transcription factor ZNF263.CONCLUSIONSThis study demonstrates that LINC00599 promotes PH progression by promoting PASMC proliferation via liquid-liquid phase separation-distinct from classical long noncoding RNA mechanisms. The identification of LINC00599 as a modulator of both m6A-dependent stress granule dynamics and MYH9-mediated phase separation expands our understanding of long noncoding RNA functionality in vascular diseases. As a target in a druggable pathway, LINC00599 holds promise for PH precision medicine.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"25 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144678273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting N6-Methyladenine of Tubular Mitochondrial DNA Against Hypertensive CKD.","authors":"Hui Liu,Ling Zhang,Zhen Lin,Zhiyuan Liu,Guangyu Hu,Xiyao Chen,Congye Li,Fangfang Sun,Xiong Guo,Chong Huang,Zhe Cui,Xinyi Wang,Zhengyang Wang,Xutong Zhang,Yile Wu,Yunlong Xia,Wenjun Yan,Shan Wang,Fuyang Zhang,Ling Tao","doi":"10.1161/hypertensionaha.124.24491","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.24491","url":null,"abstract":"BACKGROUNDHypertension is a significant global health issue that contributes to chronic kidney disease (CKD). Mitochondrial dysfunction in renal tubular epithelial cells (TECs) plays a crucial role in the progression of CKD. However, the involvement of mitochondrial DNA (mtDNA) methylation in hypertensive CKD and its potential as a therapeutic target remains largely unexamined.METHODS/RESULTSUtilizing high-confidence Nanopore sequencing, we identified N6-methyladenine (6mA) as the predominant methylation type in renal mtDNA, rather than 5-methylcytosine. In mice with hypertensive CKD induced by AngII (angiotensin II) infusion, renal mtDNA 6mA levels significantly increased, while 5-methylcytosine levels remained stable. METTL4 (methyltransferase-like protein 4), the only known mammalian methyltransferase for 6mA, was upregulated in the renal tubules of hypertensive CKD mice and patients with hypertension. AngII stimulation increased METTL4 expression and mtDNA 6mA levels in primary TECs. Activated c-Jun/AP-1 (activator protein-1) directly promoted Mettl4 transcription in AngII-treated primary TECs. METTL4-catalyzed mtDNA 6mA impeded mitochondrial transcription initiation complex assembly, thereby halting mtDNA transcription, disrupting mitochondrial function, and resulting in the transition of TECs into a proinflammatory and profibrotic phenotype. TEC-specific Mettl4 gene deletion in mice exhibited reduced mtDNA 6mA, preserved mtDNA transcription, improved tubular mitochondrial function, and alleviation of hypertensive CKD.CONCLUSIONSThis study reveals that METTL4-catalyzed mtDNA 6mA contributes to renal mitochondrial dysfunction and hypertensive CKD, offering novel therapeutic strategies from the perspective of mitochondrial epigenetics.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"24 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144652794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension and the Gut Microbiome: A Science Advisory From the American Heart Association.","authors":"Tao Yang,Katherine A Maki,Francine Z Marques,Jun Cai,Bina Joe,Carl J Pepine,Jennifer L Pluznick,Katie A Meyer,Annet Kirabo,Brian J Bennett, ","doi":"10.1161/hyp.0000000000000247","DOIUrl":"https://doi.org/10.1161/hyp.0000000000000247","url":null,"abstract":"Although substantial advancements have been made in hypertension research, translation of this research into new pharmacotherapies remains challenging. The need for new therapies is imperative: 15% to 20% of patients with hypertension have treatment-resistant hypertension, which often persists despite aggressive clinical treatments consisting of ≥3 medication classes, including a diuretic. Numerous preclinical studies have demonstrated that alterations in the gut microbiome affect blood pressure, suggesting an important role for this nonconventional cardiovascular risk factor. This innovative association suggests a novel therapeutic opportunity for hypertension: modifying the gut microbiome to control hypertension. In line with this hypothesis, clinical trials have been launched to examine whether hypertension can be managed by targeting the gut microbiome. This American Heart Association Science Advisory aims to outline clinical evidence, raise awareness among the health care community about the importance of the gut microbiome in patients with hypertension, update existing knowledge, identify research gaps, and ultimately facilitate the rapid translation of findings into clinical trials and practice.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"6 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reliability of Blood Pressure Measurement After Arteriovenous Fistula Closure in Kidney Transplant Recipients.","authors":"Yara Fares,Margaux Van Wynsberghe,Dominique Bertrand,Steven Grange,Charlotte Laurent,Dominique Guerrot,Tristan de Nattes","doi":"10.1161/hypertensionaha.125.25081","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25081","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"109 1","pages":"e154-e156"},"PeriodicalIF":8.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simplifications of the Standardized BP Measurement Procedure and Accuracy: The SIMPLE-AOBP Randomized Cross-Over Trial.","authors":"Rémi Goupil,Mérédith Lacasse,Dean S Picone","doi":"10.1161/hypertensionaha.125.25079","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25079","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"4 1","pages":"e157-e159"},"PeriodicalIF":8.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Constructing a Preeclampsia Organoid Model to Elucidate the Mechanism of Aspirin.","authors":"Shengbo Huang,Yuanjin Zhang,Yuanqing Guo,Yi Zhang,Junze Huang,Yujia Yang,Qifan Qi,Luping Zhao,Xin Xu,Yifei Shen,Chenmeizi Liang,Bingyi Yao,Xin Wang","doi":"10.1161/hypertensionaha.125.25342","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25342","url":null,"abstract":"BACKGROUNDPreeclampsia is a life-threatening pregnancy disorder characterized by hypertension and multiorgan dysfunction, posing significant risks to both maternal and fetal health. Although low-dose aspirin is widely recommended for preventing preeclampsia, the underlying mechanisms of action are still poorly understood, which hinders the optimization of therapeutic strategies.METHODSWe developed an in vitro hypoxia-induced preeclampsia model using human trophoblast organoids to replicate key pathological features. RNA sequencing identified dysregulated pathways and molecular targets. Functional assays assessed the effects of aspirin on trophoblast proliferation, mitochondrial activity, and hormonal regulation, focusing on the PI3K-AKT pathway and CYP (cytochrome P450) enzymes. We also analyzed the effects of aspirin in the N'-nitro-L-arginine-methyl ester hydrochloride rat models.RESULTSThe hypoxia-induced preeclampsia model successfully mimicked clinical hallmarks, including elevated sFLT-1 (soluble fms-like tyrosine kinase 1)/PlGF (placental growth factor) ratios and oxidative damage. RNA sequencing revealed significant suppression of the PI3K-AKT-mTOR pathway and dysregulation of CYP enzymes. Aspirin treatment restored the sFLT-1/PlGF balance, reactivated the PI3K-AKT-mTOR pathway, and improved mitochondrial function, enhancing trophoblast proliferation. Furthermore, aspirin regulated CYP expression by increasing CYP19A1 and inhibiting CYP1A1, thereby improving placental hormonal homeostasis.CONCLUSIONSThis study clarifies aspirin's multitarget mechanisms in alleviating preeclampsia, which include restoring the sFLT-1/PlGF balance, activating the PI3K-AKT-mTOR signaling pathway, optimizing mitochondrial function, and regulating CYP-mediated hormonal metabolism. These findings provide a mechanistic basis for aspirin's clinical effectiveness in preventing preeclampsia.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"27 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E-Cigarette Smoke Exposure Elevates Renal MR Expression and Induces BP Elevation.","authors":"Jian Wang,Bei Xu,Ying Wang,Jenny Liu,Piwen Wang,Rene Porche,Samuel Kim,Rong Yang,Xuesi M Shao,Kabirullah Lutfy,Limei Liu,Theodore C Friedman,Meisheng Jiang,Yanjun Liu","doi":"10.1161/hypertensionaha.124.23489","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.23489","url":null,"abstract":"BACKGROUNDE-cigarette use increases the risk of blood pressure (BP) elevation in users, though the underlying mechanisms remain unclear. The mineralocorticoid receptor (MR) is known to play an important role in the regulation of renal electrolyte balance and BP, and is protected by 11β-HSD2 (11β-hydroxysteroid dehydrogenase type 2). However, little is known about the effects of renal MR on e-cigarette-induced BP elevation.METHODSC57BL/6J male mice were exposed to aerosolized PBS, e-cigarettes without nicotine, and e-cigarettes with 2.4% nicotine, with concurrent exposure to either a vehicle or the MR antagonist eplerenone.RESULTSInhalation of e-cigarettes with nicotine markedly induced renal MR abundance and increased mean arterial BP in response to elevated plasma nicotine levels in C57BL/6J mice. Induction of MR by e-cigarettes was correlated with a reduction in 11β-HSD2 and activation of pSer9GSK3β (glycogen synthase kinase-3β phosphorylation) within the kidneys. In contrast, e-cigarettes increased the urinary ratio of corticosterone to 11-dehydrocorticosterone, reduced urinary sodium content, and elevated renal epithelial sodium channel expression. However, inhaling e-cigarettes without nicotine did not affect these metabolic parameters. Treatment with eplerenone normalized BP, reversed urinary metabolic profiles, and reduced epithelial sodium channel by inhibiting renal pSer9GSK3β in nicotine e-cigarette-exposed mice. In mouse renal CCD M1 cells, aerosol nicotine from e-cigarettes increased MR while decreasing 11β-HSD2, and these effects are likely via activation of pSer9GSK3β through a nicotinic receptor-mediated mechanism.CONCLUSIONSOur findings highlight the potential renal health damage from e-cigarettes and suggest that aerosol nicotine-mediated induction of MR action in the kidneys may contribute to electronic smoking-induced BP elevation.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"92 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of IKCa Channels on CD34+ Cells in Arteriole Remodeling in Angiotensin II-Induced Hypertension Model Mice.","authors":"Hai Tian,Xin Liao,Cheng Xie,Xiaolin Zhang,Guoqiang Ren,Pengwei Zhu,Yan Yang,Pengyun Li,Changli Liao,Chunshu Li,Qingbo Xu,Xiangyuan Pu,Jun Cheng","doi":"10.1161/hypertensionaha.124.24537","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.24537","url":null,"abstract":"BACKGROUNDMechanisms of endothelial repair in hypertension remain unclear. CD34+ cells are reported to contribute to vascular regeneration; however, their origin and regulation in hypertension are poorly understood. We investigated the role of IKCa channels in CD34+ cell-mediated endothelial repair during Ang II (angiotensin II)-induced arteriole remodeling.METHODSUsing inducible lineage tracing (Cd34-CreERT2; R26-tdTomato), we tracked nonbone marrow-derived CD34+ cells in hypertensive mice. Single-cell RNA sequencing, immunofluorescence, transwell migration assays, and patch-clamp techniques were used to analyze phenotypic transitions, ion channel activity, and signaling pathways. Bone marrow transplantation, the IKCa channel inhibitor TRAM-34, and the ERK (extracellular signal-regulated kinase) inhibitor PD98059 were used to validate functional mechanisms.RESULTSLineage tracing revealed that nonbone marrow-derived CD34+ cells contributed to endothelial repair under hypertensive conditions. Immunofluorescence analysis showed an increase in CD31+-tdTomato+ cells in the arterioles of Ang II-treated mice after 6 weeks, indicating improved endothelial integrity. Single-cell RNA sequencing revealed 2 subgroups of endothelial cells, one of which expressed stem cell markers such as CD34 (cluster of differentiation 34), Flk-1 (fetal liver kinase 1), and Sca-1 (stem cell antigen-1). Gene expression analysis showed that CD34+ cells are involved in endothelial repair through the regulation of cell migration. Importantly, IKCa channel activation facilitated CD34+ cell migration, and TRAM-34-based inhibition of IKCa channels reduced migration. Mechanistic studies revealed that Ang II enhanced CD34+ cell migration via IKCa-mediated activation of the ERK/P38 signaling pathway, promoting cytoskeletal reorganization and increased intracellular calcium levels.CONCLUSIONSArteriole-resident CD34+ cells contribute to endothelial repair in Ang II-induced hypertension. Moreover, IKCa channel upregulation facilitates CD34+ cell migration via ERK/P38 signaling, suggesting potential therapeutic targets for hypertension.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"21 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systolic BP Amplification: Systematic Review and Individual Participant Meta-Analysis.","authors":"Dean S Picone,Tan V Bui,Martin G Schultz,Petr Otahal,Alun D Hughes,J Andrew Black,Berend E Westerhof,Chen-Huan Chen,Fuyou Liang,Giacomo Pucci,Hao-Min Cheng,Heath Adams,Jiguang Wang,Nathan B Dwyer,Philip Roberts-Thomson,Remi Goupil,Sarang Paleri,Scott W Eaves,Xiaoqing Peng,James E Sharman","doi":"10.1161/hypertensionaha.124.24483","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.24483","url":null,"abstract":"BACKGROUNDSystolic blood pressure (SBP) amplification is a physiological phenomenon related to the level of pressure difference between the aorta and brachial artery and is associated with cuff blood pressure (BP) measurement inaccuracy. However, knowledge on the invasively measured level of aortic-to-brachial SBP amplification is limited. This study aimed to explore this, as well as anticipated effects on hypertension classification.METHODSA systematic review and individual participant data meta-analysis identified invasive brachial and aortic BP recorded in 1151 participants (62±12 years, 72% male). SBP amplification was calculated as brachial SBP minus aortic SBP. Hypertension classification (defined according to previously described thresholds for brachial and aortic BP) was compared between the aortic and brachial BP measures.RESULTSThere was a wide range of SBP amplification, which was similar between male and female (mean±SD, 8±9 mm Hg and 7±10 mm Hg, respectively) and decreased with increasing age. High SBP amplification (>15 mm Hg) was observed in 17.4% (male, 16.8% versus female, 19.5%; P=0.44), and low SBP amplification (<5 mm Hg) in 37.3% of participants (male, 37.2% versus female, 37.4%; P=0.95). The overall level of agreement between hypertension classification based on brachial and aortic BP was moderate (κ, 0.67; P<0.001; agreement, 87.4%). Agreement in hypertension classification was 65.0%, 38.1%, and 92.7% across classifications of optimal, prehypertension, and hypertension, respectively.CONCLUSIONSIn males and females there is wide variability in aortic-to-brachial SBP amplification. There were major theoretical differences in hypertension classification based on brachial versus aortic BP. This knowledge may help toward innovations for improving cuff BP measurement accuracy.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"47 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144521342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}