Hypertension最新文献

{"title":"Associations of Lipid-Lowering Drugs With Blood Pressure and Fasting Glucose: A Mendelian Randomization Study.","authors":"Beiping Song, Lulu Sun, Xiaoli Qin, Jiawen Fei, Quan Yu, Xinyue Chang, Yu He, Yi Liu, Mengyao Shi, Daoxia Guo, Ouxi Shen, Zhengbao Zhu","doi":"10.1161/HYPERTENSIONAHA.124.23829","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23829","url":null,"abstract":"<p><strong>Background: </strong>Observational studies have linked LDL-C (low-density lipoprotein-cholesterol)-lowering drugs with lower blood pressure (BP) and higher fasting glucose, but the causality remains unclear. We conducted a drug target Mendelian randomization study to assess the causal associations of genetically proxied inhibition of HMGCR (3-hydroxy-3-methylglutaryl coenzyme A reductase), PCSK9 (proprotein convertase subtilisin/kexin type 9), and NPC1L1 (Niemann-Pick C1-Like 1) with BP and fasting glucose.</p><p><strong>Methods: </strong>Single-nucleotide polymorphisms in <i>HMGCR</i>, <i>NPC1L1</i>, and <i>PCSK9</i> associated with LDL-C in a genome-wide association study meta-analysis from the Global Lipid Genetics Consortium (173 082 European individuals) were used to proxy LDL-C-lowering drug targets. BP and fasting glucose data were obtained from genome-wide association studies conducted by the International Consortium of Blood Pressure (757 601 European participants) and the Glucose and Insulin-related Traits Consortium (58 074 European participants). We used the inverse-variance weighted method and a series of sensitivity analyses for assessment.</p><p><strong>Results: </strong>Genetically proxied inhibition of HMGCR was negatively associated with systolic BP (β, -0.81 [95% CI, -1.26 to -0.37 mm Hg]; <i>P</i>=3.72×10^-⁴) and diastolic BP (β, -1.58 [95% CI, -2.24 to -0.91 mm Hg]; <i>P</i>=3.23×10^-⁶). Conversely, we observed a positive association between genetically proxied inhibition of HMGCR and high fasting glucose (β, 0.13 [95% CI, 0.08-0.17 mmol/L]; <i>P</i>=4.25×10^-⁸). However, there was no association of PCSK9 and NPC1L1 inhibition with BP or fasting glucose.</p><p><strong>Conclusions: </strong>Genetically proxied inhibition of HMGCR was significantly associated with low BP and high fasting glucose, while there was no effect of PCSK9 and NPC1L1 inhibition on BP or fasting glucose.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"743-751"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122773","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":"Progressive Increase in Renal Sympathetic Nerve Activity Induced by Cold Exposure.","authors":"Misa Yoshimoto, Kana Yagi, Shizuka Ikegame, Kenju Miki","doi":"10.1161/HYPERTENSIONAHA.124.23499","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23499","url":null,"abstract":"<p><strong>Background: </strong>Exposure to cold environments is linked to cold-induced hypertension due to activated sympathetic nerve activity (SNA) and arterial baroreceptor reflex dysfunction. However, direct measurement of SNA during cold-induced hypertension and changes in baroreflex control of SNA remain unexplored.</p><p><strong>Methods: </strong>Chronically instrumented rats were exposed to cold temperatures (10 °C) over 4 days after a control period (24 °C), and renal and lumbar sympathetic nerve activities were simultaneously measured during cold-induced hypertension. Baroreflex curves for renal SNA (RSNA) and lumbar SNA and heart rate were generated by altering arterial pressure via a bolus intravenous infusion of vasoactive drugs.</p><p><strong>Results: </strong>RSNA increased immediately after cold exposure, increased progressively throughout the 4-day period, and remained high after the cold exposure ended. Cold exposure shifted the RSNA baroreflex curve to the right and upward, gradually increasing the upper plateau (maximum capacity of sympathetic drive). The upper plateau remained elevated even after the cold exposure ended. Conversely, cold exposure increased lumbar SNA, heart rate, and arterial pressure, which subsequently returned to control levels after the cold exposure ended. These data indicate that cold exposure increases the maximum capacity to drive renal SNA in a regionally different and time-dependent manner through cumulative effects.</p><p><strong>Conclusions: </strong>Four days of cold exposure resulted in reversible effects increasing arterial pressure via lumbar SNA and heart rate, alongside time-dependent cumulative effects on RSNA. This study provides direct evidence of a self-activating pathway for RSNA that is activated by cold exposure, thus initiating cold-induced hypertension.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"615-623"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004613","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":"Autonomous Epinephrine Release by KCNJ5 Mutation Drives Familial Thoracic Aortic Aneurysm and Dissection.","authors":"Yanyu Duan, Chenglong Wu, Zhenghong Lai, Qunxing Yuan, Naixing Hu, Shaoqiang Liu, Ziyou Liu","doi":"10.1161/HYPERTENSIONAHA.124.23795","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23795","url":null,"abstract":"<p><strong>Background: </strong>The pathophysiology of familial thoracic aortic aneurysm and dissection (TAAD) is linked to genetic variants that affect aortic components. Although hypertension is a risk factor for TAAD, the precise genetic link remains unclear.</p><p><strong>Methods: </strong>A family with autosomal dominant TAAD complicated by hypertension was studied to identify candidate mutations. The effect of the identified mutation on TAAD development was investigated using a clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9-generated knock-in mouse model to elucidate the mechanism underlying hypertension-induced TAAD.</p><p><strong>Results: </strong>The <i>KCNJ5</i> p.R242Q mutation was identified in the family and met the criteria for cosegregation, rarity, and conservation. Utilizing our mouse model, we observed that a significant proportion of heterozygous mice with the mutation displayed dilated thoracic aortas. The mutation's allele dose was positively correlated with TAAD incidence following β-aminopropionitrile monofumarate treatment. Pathological changes in the thoracic aorta, including collagen deposition and dilation, elevated transforming growth factor-β activity, and extracellular matrix remodeling, were associated with hypertension. Furthermore, the mutation was found to induce lifelong isolated systolic hypertension, attributable to autonomous epinephrine secretion from the adrenal medulla. Unlike wild-type, mutated <i>KCNJ5</i> was highly expressed in the adrenal medulla instead of the adrenal cortex. Treatment with the adrenergic β-receptor blocker propranolol reduced systolic hypertension and mitigated TAAD in the heterozygous mice.</p><p><strong>Conclusions: </strong>Familial TAAD may stem from <i>KCNJ5</i> dysfunction in the G-protein-coupling domain, causing isolated systolic hypertension via increased epinephrine secretion and disruption of thoracic aortic homeostasis. These findings establish a genetic link between systolic hypertension and TAAD.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"752-764"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189190","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":"Role of Inflammatory Biomarkers in Mediating Causal Effect of Life Course Body Composition on Hypertension.","authors":"Liwan Fu, Yan Li, Hong Cheng, Jingfan Xiong, Pei Xiao, Hongbo Dong, Xinying Shan, Yanyan Li, Jie Mi","doi":"10.1161/HYPERTENSIONAHA.124.24542","DOIUrl":"10.1161/HYPERTENSIONAHA.124.24542","url":null,"abstract":"<p><strong>Background: </strong>The mediating role of inflammatory biomarkers in the causal relationship between body composition and hypertension remains unclear and requires further investigation.</p><p><strong>Methods: </strong>This study used a combination of retrospective observational analysis and Mendelian randomization approaches. Observational data were derived from 4717 Chinese children and adolescents aged 6 to 18 years who underwent dual-energy X-ray absorptiometry to assess body composition. Mendelian randomization analyses utilized summary statistics from large-scale data sets, including UK Biobank, deCODE2021, International Consortium of Blood Pressure, FinnGen, and other consortia. The inflammatory biomarkers included leptin, insulin, adiponectin, osteocalcin, FGF23 (fibroblast growth factor 23), and PTH (parathyroid hormone).</p><p><strong>Results: </strong>The observational analysis revealed that increased fat mass positively influenced diastolic blood pressure through osteocalcin, while fat-free mass had an inverse effect. Insulin mediated the association between fat mass and systolic blood pressure, diastolic blood pressure, and hypertension, with additional indirect effects observed for PTH (all <i>P</i><0.05). The Mendelian randomization analyses demonstrated a causal relationship between childhood body mass index and hypertension mediated by insulin (indirect effect: odds ratio, 0.87 [95% CI, 0.78-0.97]) and adiponectin (odds ratio, 1.13 [95% CI, 1.04-1.23]). Adiponectin mediated the effects of fat-free mass (odds ratio, 0.81 [95% CI, 0.71-0.93]) and fat mass (odds ratio, 1.30 [95% CI, 1.11-1.51]) on hypertension. Leptin, adiponectin, and insulin also mediated the causal effects of body composition on systolic blood pressure, diastolic blood pressure, and hypertension.</p><p><strong>Conclusions: </strong>These findings indicate that body composition influences blood pressure through distinct inflammatory biomarkers. Targeting inflammatory biomarkers may provide tailored strategies for managing body composition and hypertension.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e57-e69"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399107","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":"The Long-Term Blood Pressure Trends Following a Remote Hypertension Intervention: A Secondary Analysis of the Digital Care Transformation - Remotely Delivered Hypertension Management Program.","authors":"Shahzad Hassan, Alexander J Blood, David Zelle, Sanjay Kumar, Kavishwar Wagholikar, Daniel Gabovitch, Christopher P Cannon, Naomi Fisher, Benjamin M Scirica","doi":"10.1161/HYPERTENSIONAHA.124.24475","DOIUrl":"10.1161/HYPERTENSIONAHA.124.24475","url":null,"abstract":"<p><strong>Background: </strong>Hypertension is a major cardiovascular risk factor, yet traditional care often results in suboptimal blood pressure (BP) control at the population level. We implemented a remote hypertension management program that monitored home BP and titrated medications per algorithm. This study assessed the program's long-term effects by examining participants' office BP up to 42 months post-enrollment.</p><p><strong>Methods: </strong>Participants of the remote hypertension program were categorized into 4 groups: (1) enrolled-maintenance (achieved goal home BP of ≤130/80 mm Hg), (2) enrolled-early exit (left before achieving goal BP), (3) education-only (lifestyle modifications and medications compliance), and (4) white coat hypertension group (high office BP but normal home BP). Office BP readings of participants were collected up to 42 months post-enrollment. A linear mixed-effects regression model estimated mean BP levels and studied factors associated with above-goal systolic BP in the maintenance group.</p><p><strong>Results: </strong>Office BP readings from 3601 participants (mean age, 61±11 years; 57% female; 60% white; 52% atherosclerotic cardiovascular disease) were extracted from electronic health records and analyzed. All groups sustained office BP below their qualifying values (<i>P</i><0.001) over 42 months. In the maintenance group, 89.7% of participants maintained systolic BP at goal, compared with 63.5% in the early exit group, 69.4% in the education-only group, and 90.7% in the white coat hypertension group. Age >50 years was associated with above-goal systolic BP in the maintenance group.</p><p><strong>Conclusions: </strong>Participants who achieved BP control through the remote hypertension program maintained goal systolic BP in 90% of cases up to 42 months post-enrollment. These findings highlight the long-term benefits of remote, intensive management programs for effective hypertension control.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"733-742"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065365","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":"Ripple Effects of Early Life Stress on Vascular Health.","authors":"Cailin E Kellum, Gillian C Kelly, Jennifer S Pollock","doi":"10.1161/HYPERTENSIONAHA.124.17804","DOIUrl":"10.1161/HYPERTENSIONAHA.124.17804","url":null,"abstract":"<p><p>The term early life stress encompasses traumatic events occurring before the age of 18 years, such as physical abuse, verbal abuse, household dysfunctions, sexual abuse, childhood neglect, child maltreatment, and adverse childhood experiences. Adverse psychological experiences in early life are linked to enduring effects on mental and physical health in adulthood. In this review, we first describe the effects and potential mechanisms of early life stress on the components of the vasculature. Next, we dive into the impact of early life stress on the vasculature across the lifespan through alterations of the epigenetic landscape. Finally, we consolidate the critical gaps in knowledge for focusing future research including the potential for resilience in combatting the impact of early life stress on vascular health.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"549-560"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065372","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":"Downregulated PSME3 Contributes to Severe Preeclampsia by Promoting Trophoblast Cell Apoptosis.","authors":"Lin Liu, Hui Chen, Renfei Wu, Qiongyao Wang, Qiujing Guan, Yang Chen, Siyuan Cao, Longying Tang, Zaijun Lin, Lei Li, Xiaoli Ge","doi":"10.1161/HYPERTENSIONAHA.124.22718","DOIUrl":"10.1161/HYPERTENSIONAHA.124.22718","url":null,"abstract":"<p><strong>Background: </strong>Severe preeclampsia (sPE) is a serious condition posing risks to both maternal and fetal health. Based on mass spectrometry analysis, we identified a key protein, PSME3 (proteasome activator subunit 3), an 11S proteasome activator, whose protein level was significantly downregulated in sPE placentas and whose function in sPE remains unknown.</p><p><strong>Methods: </strong>PSME3 protein levels in human placental tissue were detected using Western blot, and PSME3 concentration in serum was detected by ELISA assay. The human preeclampsia-like phenotypes of <i>Psme3</i>^-^<i>/</i>- pregnant mice were examined. Trophoblast cell apoptosis was detected by flow cytometry. Pregnant mice were treated with 9.5% O₂ to construct a preeclampsia mouse model for detecting placental Psme3 expression. The regulation of PSME3 expression by hypoxia was detected in trophoblast cell lines treated with 21% O₂ or 1% O₂.</p><p><strong>Results: </strong>PSME3 protein levels were significantly downregulated in sPE placentas and serum. Pregnant mice with <i>Psme3</i>^-<i>/</i>- embryos and placentas spontaneously presented human preeclampsia-like symptoms, including hypertension and proteinuria, increased serum soluble fms-like tyrosine kinase 1 concentration, fetal growth restriction, and increased cellular apoptosis. Mechanically, PSME3 knockdown promoted the apoptosis of trophoblast cells by repressing the degradation of UBE2V2 (ubiquitin conjugating enzyme E2 V2). Moreover, the placentas of hypoxia-induced preeclampsia mice presented significantly reduced Psme3 protein levels and elevated Ube2v2 protein levels. Hypoxia-inducible factor-1α functioned as a transcriptional repressor of PSME3.</p><p><strong>Conclusions: </strong>In sPE placentas, hypoxia of the placenta may lead to the transcriptional inhibition of PSME3. PSME3 deficiency promotes the accumulation of UBE2V2, thereby inducing trophoblast cell apoptosis. Our study provides a new perspective for elucidating the pathogenesis of sPE.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"690-703"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189192","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":"GWAS for Defining the Pathogenesis of Hypertension: Have They Delivered?","authors":"Matthew R Alexander, Todd L Edwards, David G Harrison","doi":"10.1161/HYPERTENSIONAHA.124.23451","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23451","url":null,"abstract":"<p><p>Genome-wide association studies have identified >3500 associated single nucleotide polymorphisms and over 1000 independent loci associated with hypertension. These individually have small effect sizes, and few associated loci have been experimentally tested for causal roles in hypertension using animal models or in humans. Thus, methods to prioritize and maximize the relevance of identified single nucleotide polymorphisms and associated loci are critical to determine their importance in hypertension. We propose several approaches to aid in these efforts, including: (1) integration of genome-wide association study data with multiomic data sets, including proteomics, transcriptomics, and epigenomics, (2) utilizing linked clinical and genetic data sets to determine genetic contributions to hypertension subphenotypes with distinct drivers, and (3) performing whole exome/genome sequencing on cohorts of individuals with severe hypertension to enrich for rare variants with larger effect sizes. Rather than creating longer lists of hypertension-associated single nucleotide polymorphisms, these approaches are needed to identify key mediators of hypertension pathophysiology.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"573-582"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11922662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399100","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":"How Low Can You Go? Flagging a Role for Hypotension in Cognitive Decline With Intensive Blood Pressure Therapy.","authors":"Clinton B Wright, Hyun Song","doi":"10.1161/HYPERTENSIONAHA.125.24639","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.125.24639","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"82 4","pages":"638-639"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663567","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":"ACE Inhibition to Distinguish Low-Renin Hypertension From Primary Aldosteronism.","authors":"Cheng-Hsuan Tsai, Jenifer M Brown, Stefanie Parisien-La Salle, Andrew Newman, Vin-Cent Wu, Yen-Hung Lin, Anand Vaidya","doi":"10.1161/HYPERTENSIONAHA.125.24711","DOIUrl":"10.1161/HYPERTENSIONAHA.125.24711","url":null,"abstract":"<p><strong>Background: </strong>Primary aldosteronism (PA) is a distinct cause of low-renin hypertension (LRH), characterized by inappropriate aldosterone production. We investigated the distinction between LRH and PA by leveraging the physiological effects of angiotensin-converting enzyme inhibition.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study including 756 patients with LRH who underwent a captopril challenge test (CCT) for evaluation of PA. The distinction between PA and LRH was assessed using 4 CCT criteria: (1) Post-CCT plasma renin activity <1 ng/mL per hour and plasma aldosterone concentration decrease <30%; (2) Post-CCT aldosterone-to-renin ratio (ARR) >30 ng/dL per ng/mL per hour; (3) Post-CCT plasma renin activity <1 ng/mL per hour; and (4) Post-CCT plasma aldosterone concentration >11 ng/dL. Longitudinal outcomes following aldosterone-targeted therapy were assessed using the Primary Aldosteronism Surgery Outcome and Primary Aldosteronism Medical Outcome criteria.</p><p><strong>Results: </strong>There was a continuous spectrum of nonsuppressible aldosterone production post-CCT. When interpreting CCT results based on both renin and aldosterone responses (criteria 1 or 2), 57.8% to 66.3% of patients were classified as having PA. In contrast, when based on aldosterone or renin responses alone (criteria 3 or 4), 82.5% to 95.1% of patients were classified as having PA. Complete or partial treatment response rates following aldosterone-targeted therapy were high, ranging from 86.5% to 91.7%, regardless of CCT interpretation.</p><p><strong>Conclusions: </strong>These findings highlight the blurred distinction between LRH and PA. Although persistently suppressed renin, or elevated aldosterone, following captopril facilitated the maximum capture of PA cases, the implementation of aldosterone-targeted therapy provided similar benefits to all patints, regardless of CCT interpretation. Empirical aldosterone-directed therapy for patients with LRH suspected of having PA may be an appropriate alternative to laborious diagnostics to confirm PA.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752431","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}