Hypertension最新文献

{"title":"What Is New in the ESC Hypertension Guideline?","authors":"Jordana B Cohen","doi":"10.1161/HYPERTENSIONAHA.124.23724","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23724","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"11-13"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142285905","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":"UBR1 Promotes Sex-Dependent ACE2 Ubiquitination in Hypertension.","authors":"Mona Elgazzaz, Navya Lakkappa, Clara Berdasco, Uma Priya Mohan, Anna Nuzzo, Luke Restivo, Alexa Martinez, Amy Scarborough, Jessie J Guidry, Srinivas Sriramula, Jiaxi Xu, Hisham Daoud, Michelle A Mendiola Plá, Dawn E Bowles, Andreas M Beyer, Franck Mauvais-Jarvis, Xinping Yue, Catalin M Filipeanu, Eric Lazartigues","doi":"10.1161/HYPERTENSIONAHA.124.23196","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23196","url":null,"abstract":"<p><strong>Background: </strong>Ang-II (angiotensin II) impairs the function of the antihypertensive enzyme ACE2 (angiotensin-converting enzyme 2) by promoting its internalization, ubiquitination, and degradation, thus contributing to hypertension. However, few ACE2 ubiquitination partners have been identified, and their role in hypertension remains unknown.</p><p><strong>Methods: </strong>Proteomics and bioinformatic analyses were used to identify ACE2 ubiquitination partners in the brain, heart, and kidney of hypertensive C57BL6/J mice of both sexes. The interaction between UBR1 (ubiquitin protein ligase E3 component N-recognin) and ACE2 was validated in cells. Central and peripheral UBR1 knockdown was then performed in male mice to investigate its role in the maintenance of hypertension.</p><p><strong>Results: </strong>Proteomics analysis of the hypothalamus identified UBR1 as a potential E3 (ubiquitin protein ligase) ligase promoting ACE2 ubiquitination. Enhanced UBR1 expression, associated with ACE2 reduction, was confirmed in various tissues from hypertensive male mice and human samples. Treatment of endothelial and smooth muscle cells with testosterone, but not 17β-estradiol, confirmed a sex-specific regulation of UBR1. In vivo silencing of UBR1 using chronic administration of small interference RNA resulted in the restoration of ACE2 levels in hypertensive male mice. A transient decrease in blood pressure after intracerebroventricular, but not systemic, infusion was also observed. Interestingly, UBR1 knockdown increased brain activation of Nedd4-2 (neural precursor cell expressed developmentally downregulated protein 4), an E3 ligase promoting ACE2 ubiquitination, and reduced expression of serum and glucocorticoid-regulated kinase 1, the kinase that inactivates Nedd4-2.</p><p><strong>Conclusions: </strong>These data demonstrate that UBR1 is a novel E3 ubiquitin ligase targeting ACE2 in hypertension. UBR1 and Nedd4-2 appear to work synergistically to ubiquitinate ACE2. Targeting these ubiquitin ligases may represent a novel strategy to restore ACE2 compensatory activity in hypertension.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"84-95"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142728069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebral Blood Flow Dynamics in Neurogenic Orthostatic Hypotension: A Systematic Review and Meta-Analysis.","authors":"Jacquie R Baker, Paul A Beach, Shaun I Ranada, Aishani Patel, Jennifer Gewandter, Can Ozan Tan, Roy Freeman, Satish R Raj","doi":"10.1161/HYPERTENSIONAHA.124.23188","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23188","url":null,"abstract":"<p><strong>Background: </strong>Neurogenic orthostatic hypotension (nOH) causes pathological falls in standing blood pressure that may or may not be symptomatic. nOH also raises the risk of poor neurological outcomes irrespective of symptom presence, possibly reflecting subclinical cerebral hypoperfusion. Dynamic changes in cerebral blood flow velocity (CBFv) help infer how blood pressure fluctuations influence CBFv and cerebral autoregulation. Whether CBFv is impacted in nOH relative to related conditions without nOH and healthy controls (HC) remains unresolved. Whether nOH symptoms reflect greater CBFv falls is also unclear. This review aimed to compare CBFv between nOH and HC, nOH and disease-matched controls (eg, Parkinson disease±nOH), and between symptomatic and asymptomatic nOH.</p><p><strong>Methods: </strong>Embase and MEDLINE were searched up to April 2024. Means, SDs, and sample sizes for supine and upright CBFv were extracted to generate standardized effect sizes (Hedge g). Random-effects modeling compared postintervention between-group effect sizes.</p><p><strong>Results: </strong>Seventeen studies were included for review. Thirteen studies were suitable for meta-analysis comparing nOH to HC, 2 comparing disease-matched controls to nOH and to HC, and 3 for symptomatic comparisons. Compared with HC, nOH had larger drops in CBFv (Hedge g, -0.64 [95% CI, -0.85 to -0.44]; <i>P</i><0.001). CBFv falls between nOH and disease-matched controls were similar (<i>P</i>=0.17). Symptomatic nOH had larger CBFv drops (Hedge g, 0.84 [95% CI, 0.212-1.461]; <i>P</i>=0.009) than asymptomatic nOH.</p><p><strong>Conclusions: </strong>nOH causes significant orthostatic reductions in CBFv compared with HC, and symptomatic patients experience greater falls in CBFv than asymptomatic patients. Recognizing the clinical implications of CBFv in nOH is crucial for mitigating adverse outcomes.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"106-117"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editors and Editorial Board.","authors":"","doi":"10.1161/HYP.0000000000000244","DOIUrl":"https://doi.org/10.1161/HYP.0000000000000244","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"82 1","pages":"1-2"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854130","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":"Brief Review and Primer of Key Terminology for Artificial Intelligence and Machine Learning in Hypertension.","authors":"Patrick Dunn, Asif Ali, Akash P Patel, Srikanta Banerjee","doi":"10.1161/HYPERTENSIONAHA.123.22347","DOIUrl":"10.1161/HYPERTENSIONAHA.123.22347","url":null,"abstract":"<p><p>Recent breakthroughs in artificial intelligence (AI) have caught the attention of many fields, including health care. The vision for AI is that a computer model can process information and provide output that is indistinguishable from that of a human and, in specific repetitive tasks, outperform a human's capability. The 2 critical underlying technologies in AI are used for supervised and unsupervised machine learning. Machine learning uses neural networks and deep learning modeled after the human brain from structured or unstructured data sets to learn, make decisions, and continuously improve the model. Natural language processing, used for supervised learning, is understanding, interpreting, and generating information using human language in chatbots and generative and conversational AI. These breakthroughs result from increased computing power and access to large data sets, setting the stage for releasing large language models, such as ChatGPT and others, and new imaging models using computer vision. Hypertension management involves using blood pressure and other biometric data from connected devices and generative AI to communicate with patients and health care professionals. AI can potentially improve hypertension diagnosis and treatment through remote patient monitoring and digital therapeutics.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"26-35"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619871","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":"Mechanistic Insights Into Redox Damage of the Podocyte in Hypertension.","authors":"Daria V Ilatovskaya, Amanda Behr, Alexander Staruschenko, Gentzon Hall, Oleg Palygin","doi":"10.1161/HYPERTENSIONAHA.124.22068","DOIUrl":"10.1161/HYPERTENSIONAHA.124.22068","url":null,"abstract":"<p><p>Podocytes are specialized cells within the glomerular filtration barrier, which are crucial for maintaining glomerular structural integrity and convective ultrafiltration. Podocytes exhibit a unique arborized morphology with foot processes interfacing by slit diaphragms, ladder-like, multimolecular sieves, which provide size and charge selectivity for ultrafiltration and transmembrane signaling. Podocyte dysfunction, resulting from oxidative stress, dysregulated prosurvival signaling, or structural damage, can drive the development of proteinuria and glomerulosclerosis in hypertensive nephropathy. Functionally, podocyte injury leads to actin cytoskeleton rearrangements, foot process effacement, dysregulated slit diaphragm protein expression, and impaired ultrafiltration. Notably, the renin-angiotensin system plays a pivotal role in podocyte function, with beneficial AT2R (angiotensin receptor 2)-mediated nitric oxide (NO) signaling to counteract AT1R (angiotensin receptor 1)-driven calcium (Ca²⁺) influx and oxidative stress. Disruption of this balance contributes significantly to podocyte dysfunction and drives albuminuria, a marker of kidney damage and overall disease progression. Oxidative stress can also lead to sustained ion channel-mediated Ca²⁺ influx and precipitate cytoskeletal disorganization. The complex interplay between GPCR (G-protein coupled receptor) signaling, ion channel activation, and redox injury pathways underscores the need for additional research aimed at identifying targeted therapies to protect podocytes and preserve glomerular function. Earlier detection of albuminuria and podocyte injury through routine noninvasive diagnostics will also be critical in populations at the highest risk for the development of hypertensive kidney disease. In this review, we highlight the established mechanisms of oxidative stress-mediated podocyte damage in proteinuric kidney diseases, with an emphasis on a hypertensive renal injury. We will also consider emerging therapies that have the potential to selectively protect podocytes from redox-related injury.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"14-25"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655258/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased TRPV4 Channel Expression Enhances and Impairs Blood Vessel Function in Hypertension.","authors":"Xun Zhang, Charlotte Buckley, Matthew D Lee, Christine Salaun, Margaret MacDonald, Calum Wilson, John G McCarron","doi":"10.1161/HYPERTENSIONAHA.124.23092","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23092","url":null,"abstract":"<p><strong>Background: </strong>Endothelial cell TRPV4 (transient receptor potential vanilloid 4) channels provide a control point that is pivotal in regulating blood vessel diameter by mediating the Ca²⁺-dependent release of endothelial-derived vasoactive factors. In hypertension, TRPV4-mediated control of vascular function is disrupted, but the underlying mechanisms and precise physiological consequences remain controversial.</p><p><strong>Methods: </strong>Here, using a comprehensive array of methodologies, endothelial TRPV4 channel function was examined in intact mesenteric resistance arteries from normotensive Wistar-Kyoto and spontaneously hypertensive rats.</p><p><strong>Results: </strong>Our results show there is a notable shift in vascular reactivity in hypertension characterized by enhanced endothelium-dependent vasodilation at low levels of TRPV4 channel activation. However, at higher levels of TRPV4 activity, this vasodilatory response is reversed, contributing to the aberrant vascular tone observed in hypertension. The change in response, from dilation to constriction, was accompanied by a shift in intracellular Ca²⁺ signaling modalities arising from TRPV4 activity. Oscillatory TRPV4-evoked IP₃ (inositol triphosphate)-mediated Ca²⁺ release, which underlies dilation, decreased, while the contraction inducing sustained Ca²⁺ rise, arising from TRPV4-mediated Ca²⁺ influx, increased. Our findings also reveal that while the sensitivity of endothelial cell TRPV4 to activation was unchanged, expression of the channel is upregulated and IP₃ receptors are downregulated in hypertension.</p><p><strong>Conclusions: </strong>These data highlight the intricate interplay between endothelial TRPV4 channel expression, intracellular Ca²⁺ signaling dynamics, and vascular reactivity. Moreover, the data support a new unifying hypothesis for the vascular impairment that accompanies hypertension. Specifically, endothelial cell TRPV4 channels play a dual role in modulating blood vessel function in hypertension.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"57-68"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11654454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transforming Hypertension Diagnosis and Management in The Era of Artificial Intelligence: A 2023 National Heart, Lung, and Blood Institute (NHLBI) Workshop Report.","authors":"Daichi Shimbo, Rashmee U Shah, Marwah Abdalla, Ritu Agarwal, Faraz S Ahmad, Gabriel Anaya, Zachi I Attia, Sheana Bull, Alexander R Chang, Yvonne Commodore-Mensah, Keith Ferdinand, Kensaku Kawamoto, Rohan Khera, Jane Leopold, James Luo, Sonya Makhni, Bobak J Mortazavi, Young S Oh, Lucia C Savage, Erica S Spatz, George Stergiou, Mintu P Turakhia, Paul K Whelton, Clyde W Yancy, Erin Iturriaga","doi":"10.1161/HYPERTENSIONAHA.124.22095","DOIUrl":"10.1161/HYPERTENSIONAHA.124.22095","url":null,"abstract":"<p><p>Hypertension is among the most important risk factors for cardiovascular disease, chronic kidney disease, and dementia. The artificial intelligence (AI) field is advancing quickly, and there has been little discussion on how AI could be leveraged for improving the diagnosis and management of hypertension. AI technologies, including machine learning tools, could alter the way we diagnose and manage hypertension, with potential impacts for improving individual and population health. The development of successful AI tools in public health and health care systems requires diverse types of expertise with collaborative relationships between clinicians, engineers, and data scientists. Unbiased data sources, management, and analyses remain a foundational challenge. From a diagnostic standpoint, machine learning tools may improve the measurement of blood pressure and be useful in the prediction of incident hypertension. To advance the management of hypertension, machine learning tools may be useful to find personalized treatments for patients using analytics to predict response to antihypertension medications and the risk for hypertension-related complications. However, there are real-world implementation challenges to using AI tools in hypertension. Herein, we summarize key findings from a diverse group of stakeholders who participated in a workshop held by the National Heart, Lung, and Blood Institute in March 2023. Workshop participants presented information on communication gaps between clinical medicine, data science, and engineering in health care; novel approaches to estimating BP, hypertension risk, and BP control; and real-world implementation challenges and issues.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"36-45"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetics of Hypertension: Additive and Interactive Effects.","authors":"Zdenka Pausova, Johanne Tremblay, Pavel Hamet","doi":"10.1161/HYPERTENSIONAHA.124.21724","DOIUrl":"10.1161/HYPERTENSIONAHA.124.21724","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"3-7"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619258","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":"Response of Blood Pressure to Renal Denervation Is Not Associated With Genetic Variants.","authors":"Christian Delles, Roland E Schmieder, Rónán Daly, Dennis Kannenkeril, Agnes Bosch, Lucas Lauder, Michael Kunz, Michael Böhm, Graham Hamilton, Raphael S Schmieder, Axel Schmid, Pawel Herzyk, Felix Mahfoud","doi":"10.1161/HYPERTENSIONAHA.124.23393","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23393","url":null,"abstract":"<p><strong>Background: </strong>Renal denervation lowers blood pressure (BP) in patients with uncontrolled hypertension. We conducted an unbiased genomic screen to identify genetic variants that may associate with BP response to renal denervation (RDN).</p><p><strong>Methods: </strong>Patients (n=268) with uncontrolled resistant hypertension (baseline BP, 166±21/90±15 mm Hg) who underwent endovascular RDN using the Symplicity catheter (Medtronic, Inc, Santa Rosa, CA) were included. Reduction in 24-hour ambulatory systolic BP was assessed at 6 months and divided into 2 groups: above and below the median response of 6.0 mm Hg, taking preintervention 24-hour ambulatory BP and regression to the mean into account. Whole exome sequencing assessing 249 669 variants, was conducted using Illumina NovaSeq technology read on a NovaSeq S4 Flow Cell device.</p><p><strong>Results: </strong>We did not identify individual gene variants associated with BP response following RDN. These findings were confirmed after adjustment for sex and in a sensitivity analysis looking at tertiles of BP response. We also explored specific variants in <i>AGT</i>, <i>ADD1</i>, ADRB1, <i>ADRB2</i>, and <i>SCNN1A</i> that have been proposed as potential candidate genes for response and found no association (all <i>P</i>>0.13). Gene ontology analysis of variants across the 2 responder groups highlighted differences in biologic processes such as cell adhesion and molecular function such as protein tyrosine kinase activity.</p><p><strong>Conclusions: </strong>The response to RDN, in terms of 24-hour BP reduction, was not associated with the genetic profile of patients with resistant hypertension. These data do not support the use of a genetic score to identify potential responders to RDN.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"118-125"},"PeriodicalIF":6.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11654447/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}