Hypertension最新文献

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Central Interaction of 2-Methoxyestradiol and Lipoxygenase in AngII-Hypertension.
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-02-04 DOI: 10.1161/HYPERTENSIONAHA.124.23905
Shubha R Dutta, Purnima Singh, Chi Young Song, Ji Soo Shin, Kafait U Malik
{"title":"Central Interaction of 2-Methoxyestradiol and Lipoxygenase in AngII-Hypertension.","authors":"Shubha R Dutta, Purnima Singh, Chi Young Song, Ji Soo Shin, Kafait U Malik","doi":"10.1161/HYPERTENSIONAHA.124.23905","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23905","url":null,"abstract":"<p><strong>Background: </strong>Our previous findings that arachidonic acid-12/15-lipoxygenase (LOX)-generated metabolite 12(S)-HETE contributes to angiotensin II (AngII)-induced hypertension and 17β-estradiol protects from AngII-induced hypertension via its cytochrome P450 (CYP)1B1-generated metabolite 2-methoxyestradiol in the paraventricular nucleus (PVN) in female mice led us to test the hypothesis that 2-methoxyestradiol acts by inhibiting the LOX/12(S)-HETE in the PVN.</p><p><strong>Methods: </strong>AngII was infused subcutaneously by osmotic pumps for 2 weeks in wild-type, LOX-knockout (LOXKO), and CYP1B1KO female mice. The blood pressure was measured by tail-cuff/radiotelemetry. Adenovirus (Ad)-GFP (green fluorescence protein)-LOX-short hairpin RNA, Ad-GFP-LOX-DNA, 12(S)-HETE, and 2-methoxyestradiol were injected selectively in PVN or intracerebroventricularly. Histological, immunohistochemical, and biochemical techniques were used to determine pathophysiological changes caused by various interventions.</p><p><strong>Results: </strong>AngII-induced hypertension that was exaggerated in CYP1B1KO compared with wild-type mice was minimized by PVN-LOX knockdown with Ad-LOX-short hairpin RNA and restored by PVN-LOX reconstitution with Ad-LOX-DNA in intact-LOXKO mice and exacerbated in ovariectomized-LOXKO mice. Furthermore, intracerebroventricular-12(S)-HETE restored AngII-induced increases in blood pressure, autonomic impairment, neuroinflammation, and renal pathogenesis in intact-LOXKO mice, which were exacerbated in ovariectomized-LOXKO mice. Intracerebroventricular-2-methoxyestradiol that reduced the LOX expression and 12(S)-HETE content in PVN minimized AngII effects mentioned above in ovariectomized-LOXKO mice transduced with intracerebroventricular-Ad-LOX-DNA.</p><p><strong>Conclusions: </strong>These data suggest that 2-methoxyestradiol protects against AngII-induced hypertension and associated pathogenesis, most likely by inhibiting LOX/12(S)-HETE actions in the PVN of female mice. Therefore, the selective LOX inhibitors or 12(S)-HETE receptor antagonists could be useful in treating hypertension and its pathogenesis in postmenopausal, hypoestrogenic women or females with ovarian failure.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e34-e46"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122787","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}
引用次数: 0
MYSM1 Mediates Cardiac Parthanatos and Hypertrophy by Deubiquitinating PARP1. MYSM1通过去泛素化PARP1介导心脏骤停和肥大
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-02-05 DOI: 10.1161/HYPERTENSIONAHA.124.23823
Xin Zhong, Jianjiang Xu, Xiaowen Shi, Yiting Lyu, Yuanyuan Qian, Zimin Fang, Zixuan Wang, Jincheng Xing, Bozhi Ye, Jiajun Xu, Jibo Han
{"title":"MYSM1 Mediates Cardiac Parthanatos and Hypertrophy by Deubiquitinating PARP1.","authors":"Xin Zhong, Jianjiang Xu, Xiaowen Shi, Yiting Lyu, Yuanyuan Qian, Zimin Fang, Zixuan Wang, Jincheng Xing, Bozhi Ye, Jiajun Xu, Jibo Han","doi":"10.1161/HYPERTENSIONAHA.124.23823","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23823","url":null,"abstract":"<p><strong>Background: </strong>Cardiac hypertrophy constitutes the primary pathological basis for heart failure and exerts a considerable influence on morbidity and mortality. Deubiquitinating enzymes are crucial regulators of protein degradation and play a pivotal role in cardiac pathophysiology. This study aimed to clarify the involvement of a deubiquitinating enzyme, MYSM1 (Myb-like, SWIRM [Swi3p, Rsc8p and Moira], and MPN [Mpr1/Pad1 N-terminal] domains 1), in cardiac hypertrophy and to explore the underlying mechanism.</p><p><strong>Methods: </strong>Cardiac hypertrophy was developed by angiotensin II or transverse aortic constriction surgery. Cardiomyocyte-specific knockdown of MYSM1 was accomplished using the adeno-associated virus serotype 9-<i>cTNT-Mysm1</i>-shRNA. Co-immunoprecipitation combined with liquid chromatography-tandem mass spectrometry analysis was utilized to identify potential substrates of MYSM1.</p><p><strong>Results: </strong>First, we discovered that the expression of MYSM1 increases during cardiac hypertrophy. MYSM1 knockdown mitigated cardiac dysfunction and hypertrophy after angiotensin II administration. Cardiomyocyte-specific knockdown of MYSM1 with adeno-associated virus serotype 9 alleviated myocardial dysfunction and hypertrophy caused by transverse aortic constriction surgery. Through co-immunoprecipitation and LC-MS, poly (ADP-ribose) polymerase 1 (PARP1) was identified as a potential substrate protein of MYSM1. PARP1 initiates a novel form of programmed cell death termed parthanatos, which is characterized by excessive PARylation, nuclear translocation of AIF, and depletion of nicotinamide adenine dinucleotide. MYSM1 deubiquitinates and stabilizes PARP1 in an MPN domain-dependent manner. In addition, MYSM1 mediates cardiac hypertrophy through PARP1-dependent cardiomyocyte parthanatos.</p><p><strong>Conclusions: </strong>This study identified the role of the MYSM1-PARP1 axis in mediating cardiac hypertrophy and suggested that MYSM1 is a promising pharmacological target for the treatment of cardiac hypertrophy.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"704-715"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189194","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}
引用次数: 0
Modulation of Calcium Signaling on Demand to Decipher the Molecular Mechanisms of Primary Aldosteronism.
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-02-12 DOI: 10.1161/HYPERTENSIONAHA.124.23295
Bakhta Fedlaoui, Teresa Cosentino, Zeina R Al Sayed, Rita Alexandre Coelho, Isabelle Giscos-Douriez, Nicolo Faedda, May Fayad, Jean-Sebastien Hulot, Christopher J Magnus, Scott M Sternson, Simon Travers-Allard, Stephanie Baron, David Penton, Fabio L Fernandes-Rosa, Maria-Christina Zennaro, Sheerazed Boulkroun
{"title":"Modulation of Calcium Signaling on Demand to Decipher the Molecular Mechanisms of Primary Aldosteronism.","authors":"Bakhta Fedlaoui, Teresa Cosentino, Zeina R Al Sayed, Rita Alexandre Coelho, Isabelle Giscos-Douriez, Nicolo Faedda, May Fayad, Jean-Sebastien Hulot, Christopher J Magnus, Scott M Sternson, Simon Travers-Allard, Stephanie Baron, David Penton, Fabio L Fernandes-Rosa, Maria-Christina Zennaro, Sheerazed Boulkroun","doi":"10.1161/HYPERTENSIONAHA.124.23295","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23295","url":null,"abstract":"<p><strong>Background: </strong>Primary aldosteronism is the most common form of secondary hypertension. The most frequent genetic cause of aldosterone-producing adenomas is somatic mutations in the potassium channel KCNJ5. They affect the ion selectivity of the channel, with sodium influx leading to cell membrane depolarization and activation of calcium signaling, the major trigger for aldosterone biosynthesis.</p><p><strong>Methods: </strong>To investigate how <i>KCNJ5</i> mutations lead to the development of aldosterone-producing adenomas, we established an adrenocortical cell model in which sodium entry into the cells can be modulated on demand using chemogenetic tools [H295R-S2 α7-5HT3-R (α7-5HT3 receptor) cells]. We investigated their functional and molecular characteristics with regard to aldosterone biosynthesis and cell proliferation.</p><p><strong>Results: </strong>A clonal cell line with stable expression of the chimeric α7-5HT3-R in H295R-S2 (human adrenocortical carcinoma cell line, Strain 2) cells was obtained. Increased sodium entry through α7-5HT3-R upon stimulation with uPSEM-817 (uPharmacologically Selective Effector Molecule-817) led to cell membrane depolarization, opening of voltage-gated Ca<sup>2+</sup> channels, and increased intracellular Ca<sup>2+</sup> concentrations, resulting in the stimulation of <i>CYP11B2</i> expression and increased aldosterone biosynthesis. Increased intracellular sodium influx did not increase proliferation but rather induced apoptosis. RNA sequencing and steroidome analyses revealed unique profiles associated with Na<sup>+</sup> entry, with only partial overlap with Ang II (angiotensin II) or potassium-induced changes.</p><p><strong>Conclusions: </strong>H295R-S2 α7-5HT3-R cells are a new model reproducing the major features of cells harboring <i>KCNJ5</i> mutations. Increased expression of <i>CYP11B2</i> and stimulation of the mineralocorticoid biosynthesis pathway are associated with a decrease of cell proliferation and an increase of apoptosis, indicating that additional events may be required for the development of aldosterone-producing adenomas.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"716-732"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399104","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}
引用次数: 0
Endothelin Antagonism: A New Era for Resistant Hypertension?
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-03-19 DOI: 10.1161/HYPERTENSIONAHA.125.24606
Gavin B Chapman, Neeraj Dhaun
{"title":"Endothelin Antagonism: A New Era for Resistant Hypertension?","authors":"Gavin B Chapman, Neeraj Dhaun","doi":"10.1161/HYPERTENSIONAHA.125.24606","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.125.24606","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"82 4","pages":"611-614"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663566","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}
引用次数: 0
Abolition of Aorticorenal Ganglia Pacing Responses Improves Denervation Efficacy.
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-01-30 DOI: 10.1161/HYPERTENSIONAHA.124.24250
Poornima Balaji, Xingzhou Liu, Vu Toan Tran, Michael A Barry, Albert Vien, Edward Yang, Duc Minh Nguyen, Urja Patel, Juntang Lu, Shirley Alvarez, Sushil Bandodkar, Winny Varikatt, Alistair McEwan, Stuart P Thomas, Pierre C Qian
{"title":"Abolition of Aorticorenal Ganglia Pacing Responses Improves Denervation Efficacy.","authors":"Poornima Balaji, Xingzhou Liu, Vu Toan Tran, Michael A Barry, Albert Vien, Edward Yang, Duc Minh Nguyen, Urja Patel, Juntang Lu, Shirley Alvarez, Sushil Bandodkar, Winny Varikatt, Alistair McEwan, Stuart P Thomas, Pierre C Qian","doi":"10.1161/HYPERTENSIONAHA.124.24250","DOIUrl":"10.1161/HYPERTENSIONAHA.124.24250","url":null,"abstract":"<p><strong>Background: </strong>Transcatheter renal denervation (RDN) remains inconsistent despite developments in ablation technologies, due to the lack of an intraprocedural physiological end point. The aim of this study was to identify if aorticorenal ganglion (ARG) guided RDN using microwave (MW) catheter leads to more consistent denervation outcomes compared with empirical MW ablation.</p><p><strong>Methods: </strong>Pigs underwent sham procedure (n=8) or bilateral RDN using an in-house built open-irrigated MW catheter. Before denervation, ipsilateral ARG pacing was performed leading to renal artery vasoconstriction. MW ablation group (MW-group; n=7) received 1 ablation (100-120 W for 360 seconds) in the mid-main renal artery based on artery caliber. ARG-guided-MW ablation group (ARG-MW-group; n=7) was permitted an additional ablation more distally or at higher power until a vasoconstrictive response was abolished. Animals were euthanized at 4 to 5 weeks post-procedure.</p><p><strong>Results: </strong>ARG pacing caused an ipsilateral reduction in renal artery caliber from 4.67 to 4 mm; <i>P</i>=0.0006 in MW-group and 4.8 to 3.9 mm; <i>P</i>=0.001 in ARG-MW-group. Repeat ARG pacing at euthanasia led to a reduction in renal artery caliber in MW-group from 5.1 to 4.8 mm; <i>P</i>=0.006, but not in ARG-MW-group from 4.88 to 4.55 mm; <i>P</i>=0.08. There were no differences in ablation injury volumes between the groups. Compared with undenervated sham controls, ARG-MW-RDN versus MW-RDN caused median reductions in viable nerve area (antityrosine hydroxylase staining) at 4 to 5 weeks by 92.6% (interquartile range, 0.94-19.59%; <i>P</i><0.0001) versus 55.02% (interquartile range, 15.87-75.11%; <i>P</i>=0.006) and median renal cortical norepinephrine content by 68.06% (interquartile range, 27.16-38.39%; <i>P</i><0.0001) versus 25.25% (interquartile range, 56.97-157.7%; <i>P</i>=NS).</p><p><strong>Conclusions: </strong>ARG pacing serves as a physiological procedural end point to guide MW denervation to improve denervation outcomes.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"680-689"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065346","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}
引用次数: 0
Aprocitentan for Blood Pressure Reduction in Black Patients. 阿普昔坦在黑人患者中的降压作用。
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-01-22 DOI: 10.1161/HYPERTENSIONAHA.124.24142
John M Flack, Markus P Schlaich, Michael A Weber, Mouna Sassi-Sayadi, Krzysztof Narkiewicz, Martine Clozel, Roland F Dreier, Nabil S Andrawis, Parisa Danaietash, Nashwa Gabra, David Scott, Ji-Guang Wang, Keith C Ferdinand
{"title":"Aprocitentan for Blood Pressure Reduction in Black Patients.","authors":"John M Flack, Markus P Schlaich, Michael A Weber, Mouna Sassi-Sayadi, Krzysztof Narkiewicz, Martine Clozel, Roland F Dreier, Nabil S Andrawis, Parisa Danaietash, Nashwa Gabra, David Scott, Ji-Guang Wang, Keith C Ferdinand","doi":"10.1161/HYPERTENSIONAHA.124.24142","DOIUrl":"10.1161/HYPERTENSIONAHA.124.24142","url":null,"abstract":"<p><strong>Background: </strong>Black individuals frequently present with resistant hypertension and disproportionately increased cardiovascular risk. We investigated the blood pressure (BP)-lowering effect of the dual endothelin receptor antagonist aprocitentan in Black individuals enrolled in the PRECISION study (Parallel-Group, Phase 3 Study with Aprocitentan in Subjects with Resistant Hypertension).</p><p><strong>Methods: </strong>Patients with confirmed resistant hypertension were randomized to aprocitentan 12.5 mg, 25 mg, or placebo for 4 weeks (part 1). They subsequently received aprocitentan 25 mg for 32 weeks (part 2) before re-randomization to aprocitentan 25 mg or placebo (part 3).</p><p><strong>Results: </strong>Eighty-two patients randomized in the PRECISION study were Black individuals. At week 4, aprocitentan 12.5 and 25 mg reduced office trough systolic BP (-11.3 and -11.9 mm Hg) to a similar degree as placebo (-12.0 mm Hg). Using 24-hour ambulatory BP monitoring, the placebo effect was minimal (-0.7 mm Hg), and aprocitentan reduced systolic BP by 4.0 and 8.6 mm Hg. During part 2, office BP continued to decrease (-16.4 mm Hg at week 36). In part 3, office and ambulatory systolic BP increased on placebo (+9.9 and +8.1 mm Hg, respectively), whereas the BP-lowering effect was maintained with aprocitentan. Aprocitentan markedly reduced albuminuria during the study. The most frequent adverse event was peripheral edema, occurring in 3 patients (10%) receiving aprocitentan 25 mg versus none receiving aprocitentan 12.5 mg or placebo.</p><p><strong>Conclusions: </strong>Aprocitentan reduced BP and albuminuria in Black individuals with resistant hypertension. The BP-lowering efficacy was similar to that of the overall PRECISION population. Aprocitentan may represent an important addition to the often difficult-to-control hypertension in Black individuals.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT03541174.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"601-610"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004611","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}
引用次数: 0
Left Out in the Cold? The Sympathetic Signature of Cold-Induced Hypertension.
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-03-19 DOI: 10.1161/HYPERTENSIONAHA.125.24634
John W Osborn, Brianna Dailey-Krempel
{"title":"Left Out in the Cold? The Sympathetic Signature of Cold-Induced Hypertension.","authors":"John W Osborn, Brianna Dailey-Krempel","doi":"10.1161/HYPERTENSIONAHA.125.24634","DOIUrl":"10.1161/HYPERTENSIONAHA.125.24634","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"82 4","pages":"624-626"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663568","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}
引用次数: 0
Pregnancy Metal Mixtures and Blood Pressure and Hypertension in Mid-Life: A Prospective U.S. Cohort Study.
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-03-06 DOI: 10.1161/HYPERTENSIONAHA.124.23980
Mingyu Zhang, Izzuddin M Aris, Andres Cardenas, Sheryl L Rifas-Shiman, Pi-I Debby Lin, Long H Ngo, Emily Oken, Marie-France Hivert, Stephen P Juraschek
{"title":"Pregnancy Metal Mixtures and Blood Pressure and Hypertension in Mid-Life: A Prospective U.S. Cohort Study.","authors":"Mingyu Zhang, Izzuddin M Aris, Andres Cardenas, Sheryl L Rifas-Shiman, Pi-I Debby Lin, Long H Ngo, Emily Oken, Marie-France Hivert, Stephen P Juraschek","doi":"10.1161/HYPERTENSIONAHA.124.23980","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23980","url":null,"abstract":"<p><strong>Background: </strong>The long-term associations between metal mixtures in pregnancy and women's mid-life blood pressure (BP) and hypertension remain unclear.</p><p><strong>Methods: </strong>In Project Viva (enrolled 1999-2002), we measured nonessential (arsenic, barium, cadmium, cesium, mercury, lead) and essential metals (copper, magnesium, manganese, selenium, zinc) in red blood cells, along with folate and vitamin B12 in plasma, collected during pregnancy. We measured mid-life BP from 2017 to 2021 (median age, 51.2 years). We examined associations of individual metals with BP using linear regression and with hypertension (≥130/80 mm Hg or use of antihypertensive medication) using modified Poisson regression. We used Bayesian kernel machine regression to examine the mixture effects of metals and micronutrients.</p><p><strong>Results: </strong>The median follow-up time of the 493 women was 18.1 years (interquartile range, 17.8-18.6 years). After adjustment, a doubling of copper and manganese was associated with 0.75 (95% CI, 0.57-0.99) and 0.80 (95% CI, 0.71-0.91) times the risk of hypertension, respectively. Although higher cesium and selenium levels were associated with a slightly increased risk of hypertension, the 95% CIs were wide and crossed the null. A doubling of vitamin B12 was associated with a 3.64 (95% CI, 1.23-6.04) mm Hg lower systolic BP and a 2.52 (95% CI, 0.72-4.32) mm Hg lower diastolic BP. Bayesian kernel machine regression showed linear associations with no metal-metal or metal-micronutrient interactions. The essential metal mixture was monotonically associated with lower BP, while its association with hypertension showed threshold effects.</p><p><strong>Conclusions: </strong>Optimizing essential metal levels during pregnancy, particularly copper and manganese, along with vitamin B12, may protect against higher BP and hypertension in mid-life women.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"640-651"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11922668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572932","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}
引用次数: 0
Channeling Hope in the Expanding Landscape of Therapy for Pulmonary Hypertension: Potential Role for Piezo2.
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-03-19 DOI: 10.1161/HYPERTENSIONAHA.125.24570
Jochen Steppan, Dan E Berkowitz
{"title":"Channeling Hope in the Expanding Landscape of Therapy for Pulmonary Hypertension: Potential Role for Piezo2.","authors":"Jochen Steppan, Dan E Berkowitz","doi":"10.1161/HYPERTENSIONAHA.125.24570","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.125.24570","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"82 4","pages":"598-600"},"PeriodicalIF":6.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663563","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}
引用次数: 0
Efficacy and Safety of Aldosterone Synthase Inhibitors for Hypertension: A Meta-Analysis of Randomized Controlled Trials and Systematic Review.
IF 6.9 1区 医学
Hypertension Pub Date : 2025-04-01 Epub Date: 2025-01-31 DOI: 10.1161/HYPERTENSIONAHA.124.23962
Luigi Marzano, Matteo Merlo, Nicola Martinelli, Francesca Pizzolo, Simonetta Friso
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