Hypertension最新文献

{"title":"Finerenone Plus Empagliflozin: How Low Can We Go, and How Much Does Blood Pressure Matter?","authors":"Carmine Zoccali, Francesca Mallamaci","doi":"10.1161/HYPERTENSIONAHA.126.27364","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.27364","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"83 9","pages":"e27364"},"PeriodicalIF":9.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792401","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":"Primary Aldosteronism Medical Treatment Outcomes (PAMO) Beyond 12 Months.","authors":"Jun Yang, Jessica Goi, Jacopo Burrello, Martin Reincke, Christian Adolf, Denise Brüdgam, Qifu Li, Ying Song, Jinbo Hu, Shumin Yang, Fumitoshi Satoh, Yoshikiyo Ono, Renata Libianto, Michael Stowasser, Nanfang Li, Qing Zhu, Namki Hong, Drishya Nayak, Troy H Puar, Vin-Cent Wu, Anand Vaidya, Marta Araujo-Castro, Tomaz Kocjan, Samuel Matthew O'Toole, Gregory L Hundemer, Oskar Ragnarsson, André Lacroix, Stephanie Larose, Kazuki Nakai, Tetsuo Nishikawa, Daria Ladygina, Adina F Turcu, Peeradon Vibhatavata, Carlos E Fardella, Thomas Uslar, Marcus Quinkler, Paolo Mulatero, Giovanni Pintus, Gian Paolo Rossi, Stefanie Hahner, Laurence Amar, William M Drake, Chetna Varsani, Morris J Brown, Xilin Wu, William F Young, Tracy Ann Williams, Peter J Fuller","doi":"10.1161/HYPERTENSIONAHA.126.27431","DOIUrl":"10.1161/HYPERTENSIONAHA.126.27431","url":null,"abstract":"<p><strong>Background: </strong>Primary aldosteronism (PA) is a common and treatable cause of hypertension, yet data on the durability of medical treatment response beyond the first year are limited. Using the PA medical treatment outcomes framework, we evaluated long-term biochemical and clinical outcomes and factors associated with treatment response.</p><p><strong>Methods: </strong>We conducted an international, multicenter, observational cohort study across 27 centers on 4 continents. Adults with PA treated with mineralocorticoid receptor antagonists and/or epithelial sodium channel blockers between 2016 and 2021 were included if follow-up data were available at ≥12 months. Biochemical and clinical responses were classified as complete, partial, or absent using PA medical treatment outcomes criteria. Ordinal logistic regression identified determinants of a favorable treatment response.</p><p><strong>Results: </strong>The cohort included 1292 patients (47.5% women, mean age 52 years) with a median follow-up of 34 months (interquartile range, 21-51). At ≥12 months, 58.3% achieved a complete biochemical response, and 20.8% achieved a complete clinical response, with only 5% showing no response. Determinants of a favorable biochemical response included lower aldosterone and lateralization index, and higher renin and potassium levels at baseline. In those taking spironolactone, a higher daily dose was also associated with a favorable biochemical response. Determinants of a favorable clinical response included female sex, lower body mass index, shorter duration of hypertension, and absence of hypertension-mediated organ damage.</p><p><strong>Conclusions: </strong>Targeted medical therapy for PA can deliver sustained biochemical and clinical benefits. Early disease detection and adequate dose titration are highly actionable determinants of long-term treatment success.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e27431"},"PeriodicalIF":9.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548767","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 High Dietary Salt on Neurovascular and Cognitive Functions.","authors":"Giuseppe Faraco","doi":"10.1161/HYPERTENSIONAHA.126.26772","DOIUrl":"10.1161/HYPERTENSIONAHA.126.26772","url":null,"abstract":"<p><p>Dietary sodium intake in most world regions substantially exceeds physiological requirements, with well-documented consequences for cardiovascular and cerebrovascular health. Although the contribution of dietary salt to blood pressure elevation is well established, evidence from both experimental and human studies indicates that excess sodium adversely affects the cerebral vasculature and cognitive function through mechanisms that operate independently of blood pressure. Here, we review this evidence, integrating findings from animal models with observational and clinical data from human studies. Rodent studies consistently demonstrate that high-salt diet impairs cerebrovascular function and promotes cognitive decline, through mechanisms including IL (interleukin)-17A-mediated endothelial nitric oxide dysfunction, tau hyperphosphorylation, and neuroinflammation. In humans, growing evidence indicates that high dietary sodium accelerates cognitive decline and cerebral small vessel disease progression, though methodological limitations preclude definitive conclusions about causality in most studies. Critically, emerging evidence suggests that the relationship between dietary sodium and cognitive aging is nonlinear, with very low intake also associated with adverse outcomes. Taken together, the available evidence supports a role for dietary sodium in cerebrovascular and cognitive dysfunction that extends beyond its pressor effects, though adequately powered longitudinal studies combining gold-standard assessment of sodium intake with neuroimaging and cognitive end points are needed to establish causality with greater confidence.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13519947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817335","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":"Blood Pressure Variability and Alzheimer Disease Biomarkers.","authors":"Trevor Lohman, Isabel Sible, Yuan Ma, Niema M Pahlevan, Daniel A Nation","doi":"10.1161/HYPERTENSIONAHA.126.26768","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.26768","url":null,"abstract":"<p><p>Increased blood pressure variability (BPV) is associated with increased risk for dementia, independent of hypertension. The increased risk for dementia associated with high BPV includes probable Alzheimer disease (AD) dementia, but high BPV is also associated with increased risk of stroke and cerebral small vessel disease, which are commonly comorbid with AD. This raises the question of whether high BPV is independently predictive of AD-specific pathophysiology and neurodegeneration, which could have significant clinical implications. Fewer studies have directly addressed this question by examining whether higher BPV predicts future AD biomarker abnormalities that are specific to AD pathophysiology within the amyloid/tau/neurodegeneration framework. This narrative review summarizes current studies on this topic and discusses future directions in the investigation of elevated BPV as a risk factor for AD, the most common cause of dementia in older adults.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792413","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":"Pregnancy Weight Gain and Longer-Term Maternal Cardiometabolic Conditions.","authors":"Thais Rangel Bousquet Carrilho, Sonia M Grandi, Lisa M Bodnar, Jennifer A Hutcheon, Kari Johansson","doi":"10.1161/HYPERTENSIONAHA.125.26320","DOIUrl":"10.1161/HYPERTENSIONAHA.125.26320","url":null,"abstract":"<p><strong>Background: </strong>We aimed to establish how weight gain patterns across successive pregnancies relate to longer-term maternal cardiometabolic health.</p><p><strong>Methods: </strong>Obstetric records of all nulliparous pregnancies in Stockholm and Gotland (Sweden, 2008-2015) were linked with hospital discharges, outpatient visits, and prescription dispensations until 2019. Total pregnancy weight gain (kg) was standardized for gestational age and early pregnancy body mass index and classified as ≤ -1, > -1 and < +1 (reference), and ≥ +1 <i>Z</i> scores. Postpartum cardiometabolic conditions (type 2 diabetes, hypertension, cardiovascular diseases) were identified using <i>International Classification of Diseases</i>, <i>Tenth Revision</i> codes and medications. Hazard ratios were estimated using a Cox proportional hazards model.</p><p><strong>Results: </strong>Among 58 333 individuals, 5.9% (n=3440) developed a cardiometabolic condition, with a median onset of 4 years [interquartile range, 2-6]. Hazard ratios were higher for those gaining ≥ +1 <i>Z</i> score (19.4 kg at 40 weeks in normal-weight individuals) in the first pregnancy (hazard ratio, 1.29 [95% CI, 1.19-1.40]). Among individuals developing conditions after the second pregnancy, risks were increased for those with high weight gain in the first pregnancy, but not the second (hazard ratios, 1.30 [95% CI, 1.13-1.50] versus 1.05 [95% CI, 0.88-1.26], respectively), compared with those gaining > -1 and < +1 <i>Z</i> score in both pregnancies.</p><p><strong>Conclusions: </strong>Individuals with high weight gain in their first pregnancy were 30% more likely to develop a cardiometabolic condition than those with lower weight gain. Preventing excessive weight gain in the first pregnancy may be key to reducing maternal cardiometabolic risk.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e26320"},"PeriodicalIF":9.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148149625","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":"Severe Acute Hypertension Causes Hemolysis With Release of PEP and ACE Inhibitor.","authors":"Romy Fischer, Jan Wysocki, Luise Hassler, Daniel Batlle","doi":"10.1161/HYPERTENSIONAHA.125.26651","DOIUrl":"10.1161/HYPERTENSIONAHA.125.26651","url":null,"abstract":"<p><strong>Background: </strong>Acute hypertensive crises can induce intravascular hemolysis, but its impact on the renin-angiotensin system remains unclear.</p><p><strong>Methods: </strong>Acute blood pressure elevations were induced in wild-type and PEP (prolyl endopeptidase)-deficient mice via Ang II (angiotensin II) injections. Systolic blood pressure, hemolysis index, and plasma enzymatic activities were evaluated. Native and cryo-hemolyzed plasma samples were incubated ex vivo with Ang II, with or without a PEP inhibitor, and Ang-(1-7; angiotensin-[1-7]) formation was measured over time. Ang II formation from Ang I (angiotensin I) was also assessed ex vivo. Plasma ACE (angiotensin-converting enzyme) protein levels were determined by Western blotting.</p><p><strong>Results: </strong>Ang II-induced blood pressure elevations led to hemolysis and a ~3.5-fold increase in plasma PEP activity, while the activities of other Ang II-degrading enzymes were unchanged. Pretreatment with recombinant ACE2 before Ang II infusion markedly attenuated both the systolic blood pressure and the hemolysis index. Cryo-hemolyzed plasma from mice and humans showed markedly increased ex vivo Ang-(1-7) formation from Ang II compared with native plasma, which was obliterated by PEP inhibition. In addition, ex vivo Ang II formation from Ang I was markedly decreased in cryo-hemolyzed plasma, and this was associated with reduced ACE activity, while ACE protein levels remained unchanged.</p><p><strong>Conclusions: </strong>Acute severe hypertension induced by Ang II infusion causes intravascular hemolysis associated with increased plasma PEP activity and decreased plasma ACE activity that, based on ex vivo findings, enhance Ang II degradation to form Ang-(1-7) and reduce Ang II formation from Ang I, respectively. These previously unrecognized effects of hemolysis on renin-angiotensin system enzymes may be involved in mechanisms that influence acute blood pressure responses.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e26651"},"PeriodicalIF":9.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13285532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148015060","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":"Complement Activation in Maternal and Placental Pathology of Preeclampsia.","authors":"Manu T Banadakoppa, Madhu S Chauhan, Moises J Tacam, Allyson W Nevins, Antonio H Ruano, Simone H Ruano, Jon A Fuson, Chandra Yallampalli","doi":"10.1161/HYPERTENSIONAHA.125.26158","DOIUrl":"10.1161/HYPERTENSIONAHA.125.26158","url":null,"abstract":"<p><strong>Background: </strong>Preeclampsia is a multifactorial, pregnancy-related disorder characterized by new-onset hypertension and proteinuria, with distinct early- and late-onset forms. Although complement dysregulation has been implicated in the pathogenesis of preeclampsia, its causal role remains unclear. In mice, Crry (complement receptor 1-related protein Y) functions as a critical complement regulator at the fetal-maternal interface. Because complete Crry deficiency is embryonically lethal, direct in vivo investigation of complement activation in pregnancy has been challenging.</p><p><strong>Methods: </strong>We generated a placenta-specific, doxycycline-inducible short hairpin RNA mouse model in which Crry expression can be downregulated in a dose-dependent manner. This system employs Cyp19-driven Cre recombinase and a tetracycline-inducible gene expression system regulatory cassette, enabling precise temporal and spatial control of Crry suppression and restricting complement activation specifically to the placenta.</p><p><strong>Results: </strong>We found that early gestation placental complement activation impairs maternal cardiac and hepatic adaptation, reduces placental efficiency, and causes fetal growth restriction-features consistent with early-onset preeclampsia. Delayed complement activation produces a phenotype resembling late-onset preeclampsia, characterized by maternal hypertension without placental pathology. In the early-onset-like phenotype, fetal growth restriction is accompanied by placental glycogen storage deficiency and impaired endocrine function. Maternal glucose metabolism remains intact; however, compensatory changes in lipid metabolism occur, although these adaptations are insufficient to prevent fetal growth restriction.</p><p><strong>Conclusions: </strong>This model demonstrates that the timing of placental complement activation determines whether pregnancy develops early- or late-onset-like features. These findings provide mechanistic insight into how complement dysregulation contributes to the spectrum of preeclampsia pathology and establish a powerful experimental platform for studying disease mechanisms and evaluating therapeutic strategies.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e26158"},"PeriodicalIF":9.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13240661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148149599","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":"β-Arrestin-2 Regulates Sodium Taste Processing.","authors":"Connie C Grobe, Autumn J Hamilton, Yada Treesukosol, Justin L Grobe, Jeffrey L Segar, Curt D Sigmund","doi":"10.1161/HYPERTENSIONAHA.126.27127","DOIUrl":"10.1161/HYPERTENSIONAHA.126.27127","url":null,"abstract":"<p><strong>Background: </strong>Altered detection and preference for sodium are associated with increased sodium intake, and increased sodium intake is associated with increased risk of hypertension. AT₁R (angiotensin II type 1 receptor) second-messenger signaling is mediated and modulated by ARRB2 (β-arrestin-2), and both AT₁R and ARRB2 in the brain influence sodium intake. Here, we examined the hypotheses that ARRB2 influences sodium taste hedonics and that these effects involve AT₁R.</p><p><strong>Methods: </strong>Sodium intake behaviors and hedonic reactions of mice carrying a null mutation of the endogenous ARRB2 gene (<i>Arrb2</i>-KO [knockout] mice) were evaluated using 2-bottle choice testing, brief-access paradigms, and intraoral taste reactivity assays.</p><p><strong>Results: </strong><i>Arrb2</i>-KO mice of both sexes exhibited dose-dependent increases in licking to sodium chloride and sucrose, but not quinine or citric acid, during a brief-access paradigm; rapid recovery of spontaneous isotonic saline intake after acute adulteration by quinine or exposure to hypertonic saline; persistently elevated isotonic saline intake even when dietary sodium content was increased from 0.15% to 1.00%; and reduced aversive reactions to acute intraoral isotonic saline. Finally, the spontaneous increase in isotonic saline intake by <i>Arrb2</i>-KO mice was abolished by administration of the AT₁R antagonist losartan.</p><p><strong>Conclusions: </strong>Together, these findings highlight a major role for ARRB2 in sodium taste processing, which appears to be mediated through an AT₁R-dependent mechanism.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e27127"},"PeriodicalIF":9.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13256247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148137888","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":"Baroreceptor Mechanotransduction: Diverse Sensors, Unified Signals.","authors":"Patrick Delmas, Nancy Osorio, Virginie Penalba, Françoise Dignat-George, Guillaume Hache","doi":"10.1161/HYPERTENSIONAHA.126.26992","DOIUrl":"10.1161/HYPERTENSIONAHA.126.26992","url":null,"abstract":"<p><p>Arterial baroreceptors constitute the safeguard of cardiovascular homeostasis by translating vascular stretch into reflex control/ afferent firing. Recent advances have identified an unexpectedly diverse palette of candidate ion channels, including PIEZO1/2, TMEM150C, TRPV1, TRPC5 (transient receptor potential canonical 5), and epithelial sodium channels (ENaC), yet the molecular logic of their mechanosensory function remains unresolved. However, the field is mired in controversy: are PIEZOs truly indispensable barosensors, or do TRPs, ENaCs, and Tentonin3 provide parallel, context-dependent mechanotransduction? Equally contentious is the extent to which distinct baroreceptor morphologies, end-net versus flower-spray terminals, rapidly versus slowly adapting afferents, deploy specialized channel repertoires to encode dynamic versus steady-state pressure stimuli. Such heterogeneity challenges prevailing reductionist models and underscores baroreception as an emergent property of distributed molecular systems rather than a single-channel solution. Here, we critically appraise molecular, anatomic, and physiological evidence to advance an unifying framework in which baroreceptor diversity is both structural and functional, shaped by channel composition, terminal architecture, and afferent excitability.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e26992"},"PeriodicalIF":9.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204392","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":"Retinal and Choroidal Metrics Are Dynamic Markers of the Maternal Vascular Response to Pregnancy.","authors":"Kathryn Hunt, Georgia R Morgan, Carlos Sanchez Soriano, Jamie Burke, Ylenia Giarratano, Charlene Hamid, Rosie Keane, Roseanna Jenks, Shona Low, Sarah Donaldson, Marisa Magennis, Baljean Dhillon, Rosemary C Townsend, Tom MacGillivray, Miguel O Bernabeu, Rebecca M Reynolds","doi":"10.1161/HYPERTENSIONAHA.126.26893","DOIUrl":"10.1161/HYPERTENSIONAHA.126.26893","url":null,"abstract":"<p><strong>Background: </strong>There is an unmet need for biomarkers that can dynamically track maternal vascular health and guide interventions in disordered pregnancies. The retina and choroid provide a window into the systemic vasculature. We aimed to characterize longitudinal trajectories of retinal and choroidal features during healthy pregnancy and explore differences associated with preeclampsia.</p><p><strong>Methods: </strong>Overall, 251 pregnant women underwent multimodal retinal imaging with color fundus photography, scanning laser ophthalmoscopy, and optical coherence tomography at multiple antenatal (12±3 or 20±3 weeks' gestation and 36±3 weeks' gestation, n=183) or a single third-trimester (36±3 weeks' gestation, n=68) time point. Retinal and choroidal vascular features were extracted using an automated pipeline. We examined gestational trajectories of these features and their associations with blood pressure change and serum angiogenic factors. Trajectories were compared for women with preeclampsia and those without placental dysfunction.</p><p><strong>Results: </strong>Significant reductions in measurements of retinal vessel caliber and density and of choroidal thickness, and increases in retinal thickness measurements, were seen over healthy pregnancy. These changes were not correlated with maternal blood pressure change. Third-trimester retinal arteriolar caliber and density were weakly correlated with placental growth factor (<i>r</i>=0.32, <i>P</i><0.001 and <i>r</i>=0.31, <i>P</i><0.001) and soluble fms-like tyrosine kinase 1 (<i>r</i>=-0.21, <i>P</i>=0.006 and <i>r</i>=-0.33, <i>P</i><0.001) levels. Preeclampsia was associated with significantly greater reductions in retinal arteriolar caliber (<i>P</i>=0.022 for right eye, <i>P</i>=0.019 for left) and density (<i>P</i><0.001 for each eye) across gestation.</p><p><strong>Conclusions: </strong>Retinal and choroidal features change throughout pregnancy, and these trajectories are altered in preeclampsia.</p><p><strong>Registration: </strong>URL: https://doi.org/10.1186/ISRCTN40843826; Unique identifier: ISRCTN40843826.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e26893"},"PeriodicalIF":9.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257986","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}