High Salt Intake Is Independently Associated With Hypertensive Target Organ Damage.
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ABSTRACT:
SUBMITTER: Imaizumi Y
PROVIDER: S-EPMC8031903 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundEpigenetic age acceleration, a measure of biological aging based on DNA methylation, is associated with cardiovascular mortality. However, little is known about its relationship with hypertensive target organ damage to the heart, kidneys, brain, and peripheral arteries.MethodsWe investigated associations between intrinsic (IEAA) or extrinsic (EEAA) epigenetic age acceleration, blood pressure, and six types of organ damage in a primarily hypertensive cohort of 1390 African Americans from the Genetic Epidemiology Network of Arteriopathy (GENOA) study. DNA methylation from peripheral blood leukocytes was collected at baseline (1996-2000), and measures of target organ damage were assessed in a follow-up visit (2000-2004). Linear regression with generalized estimating equations was used to test for associations between epigenetic age acceleration and target organ damage, as well as effect modification of epigenetic age by blood pressure or sex. Sequential Oligogenic Linkage Analysis Routines (SOLAR) was used to test for evidence of shared genetic and/or environmental effects between epigenetic age acceleration and organ damage pairs that were significantly associated.ResultsAfter adjustment for sex, chronological age, and time between methylation and organ damage measures, higher IEAA was associated with higher urine albumin to creatinine ratio (UACR, p?=?0.004), relative wall thickness (RWT, p?=?0.022), and left ventricular mass index (LVMI, p?=?0.007), and with lower ankle-brachial index (ABI, p?=?0.014). EEAA was associated with higher LVMI (p?=?0.005). Target organ damage associations for all but IEAA with LVMI remained significant after further adjustment for blood pressure and antihypertensive use (p?<?0.05). Further adjustment for diabetes attenuated the IEAA associations with UACR and RWT, and adjustment for smoking attenuated the IEAA association with ABI. No effect modification by age or sex was observed.ConclusionsMeasures of epigenetic age acceleration may help to better characterize the functional mechanisms underlying organ damage from cellular aging and/or hypertension. These measures may act as subclinical biomarkers for damage to the kidney, heart, and peripheral vasculature; however more research is needed to determine whether these relationships remain independent of lifestyle factors and comorbidities.
| S-EPMC6806502 | biostudies-literature
Project description:AimsHypertensive pregnancy is associated with increased risks of developing a range of vascular disorders in later life. Understanding when hypertensive target organ damage first emerges could guide optimal timing of preventive interventions. This review identifies evidence of hypertensive target organ damage across cardiac, vascular, cerebral, and renal systems at different time points from pregnancy to postpartum.Methods and resultsSystematic review of Ovid/MEDLINE, EMBASE, and ClinicalTrials.gov up to and including February 2023 including review of reference lists. Identified articles underwent evaluation via a synthesis without meta-analysis using a vote-counting approach based on direction of effect, regardless of statistical significance. Risk of bias was assessed for each outcome domain, and only higher quality studies were used for final analysis. From 7644 articles, 76 studies, including data from 1 742 698 pregnancies, were identified of high quality that reported either blood pressure trajectories or target organ damage during or after a hypertensive pregnancy. Left ventricular hypertrophy, white matter lesions, proteinuria, and retinal microvasculature changes were first evident in women during a hypertensive pregnancy. Cardiac, cerebral, and retinal changes were also reported in studies performed during the early and late post-partum period despite reduction in blood pressure early postpartum. Cognitive dysfunction was first reported late postpartum.ConclusionThe majority of target organ damage reported during a hypertensive pregnancy remains evident throughout the early and late post-partum period despite variation in blood pressure. Early peri-partum strategies may be required to prevent or reverse target organ damage in women who have had a hypertensive pregnancy.
| S-EPMC10767256 | biostudies-literature
Project description:We investigated the association between heart rate and its variability with the parameters that assess vascular, renal and cardiac target organ damage.A cross-sectional study was performed including a consecutive sample of 360 hypertensive patients without heart rate lowering drugs (aged 56 ± 11 years, 64.2% male). Heart rate (HR) and its standard deviation (HRV) in clinical and 24-hour ambulatory monitoring were evaluated. Renal damage was assessed by glomerular filtration rate and albumin/creatinine ratio; vascular damage by carotid intima-media thickness and ankle/brachial index; and cardiac damage by the Cornell voltage-duration product and left ventricular mass index.There was a positive correlation between ambulatory, but not clinical, heart rate and its standard deviation with glomerular filtration rate, and a negative correlation with carotid intima-media thickness, and night/day ratio of systolic and diastolic blood pressure. There was no correlation with albumin/creatinine ratio, ankle/brachial index, Cornell voltage-duration product or left ventricular mass index. In the multiple linear regression analysis, after adjusting for age, the association of glomerular filtration rate and intima-media thickness with ambulatory heart rate and its standard deviation was lost. According to the logistic regression analysis, the predictors of any target organ damage were age (OR = 1.034 and 1.033) and night/day systolic blood pressure ratio (OR = 1.425 and 1.512). Neither 24 HR nor 24 HRV reached statistical significance.High ambulatory heart rate and its variability, but not clinical HR, are associated with decreased carotid intima-media thickness and a higher glomerular filtration rate, although this is lost after adjusting for age.ClinicalTrials.gov: NCT01325064.
| S-EPMC3326700 | biostudies-literature
Project description:We aimed to evaluate the association of aortic and brachial short-term blood pressure variability (BPV) with the presence of target organ damage (TOD) in hypertensive patients. One-hundred seventy-eight patients, aged 57 ± 12 years, 33% women were studied. TOD was defined by the presence of left ventricular hypertrophy on echocardiogram, microalbuminuria, reduced glomerular filtration rate, or increased aortic pulse wave velocity. Aortic and brachial BPV was assessed by 24-hour ambulatory BP monitoring (Mobil-O-Graph). TOD was present in 92 patients (51.7%). Compared to those without evidence of TOD, they had increased night-to-day ratios of systolic and diastolic BP (both aortic and brachial) and heart rate. They also had significant increased systolic BPV, as measured by both aortic and brachial daytime and 24-hours standard deviations and coefficients of variation, as well as for average real variability. Circadian patterns and short-term variability measures were very similar for aortic and brachial BP. We conclude that BPV is increased in hypertensive-related TOD. Aortic BPV does not add relevant information in comparison to brachial BPV.
| S-EPMC8030748 | biostudies-literature
Project description:We previously showed that angiotensin II (Ang II) increases T cell production of IL-17A, and that mice deficient in IL-17A have blunted hypertension and attenuated renal and vascular dysfunction. It was recently shown that salt enhances IL-17A production from CD4+ T cells via a serum- and glucocorticoid-regulated kinase 1-dependent (SGK1-dependent) pathway. Thus, we tested the hypothesis that SGK1 signaling in T cells promotes hypertension and contributes to end-organ damage. We show that loss of T cell SGK1 results in a blunted hypertensive response to Ang II infusion by 25 mmHg. Importantly, renal and vascular inflammation is abrogated in these mice compared with control mice. Furthermore, mice lacking T cell SGK1 are protected from Ang II-induced endothelial dysfunction and renal injury. Loss of T cell SGK1 also blunts blood pressure and vascular inflammation in response to deoxycorticosterone acetate-salt (DOCA-salt) hypertension. Finally, we demonstrate that the Na+-K+-2Cl- cotransporter 1 (NKCC1) is upregulated in Th17 cells and is necessary for the salt-induced increase in SGK1 and the IL-23 receptor. These studies demonstrate that T cell SGK1 and NKCC1 may be novel therapeutic targets for the treatment of hypertension and identify a potentially new mechanism by which salt contributes to hypertension.
| S-EPMC5499362 | biostudies-literature
Project description:BackgroundHypertension and its complications are among the major health problems all over the world, particularly in developing countries. The aims of this study were to show that, weather the hypertensive patients follow the expertise recommendations and differences between men and women in their levels of knowledge and behavior in salt taking.MethodsThe present cross-sectional study was conducted among all hypertensive patients in rural health centers of Tabriz, Iran, in Feb-May; 2016. Data were collected by an interviewer-administrated questionnaire, along with anthropometric, blood pressure, and 24-hour urinary sodium excretion measurements. Multivariate logistic regression analysis was used to compute adjusted odds ratio (OR).ResultsIn all 205 patients, 62.9% female, 40.5% aged over 60 years, and 53.7% with low or moderate socioeconomic status, 49.3% body mass index (BMI) 30 kg/m2 and above, 10.2% of the patients had systolic/diastolic equal and above (≥) 40/90 mmHg, participated in the study. In total, 16.6% were aware of the daily salt allowance for healthy people with sex difference (P < 0.001). Significant predictors of adding salt beyond the dietary recommendations in food preparation were occupation (unemployed) (OR = 4.05, 95% CI = 1.041-15.78, (P = 0.044)) and blood pressure level (systolic/diastolic ≥140/90) (OR = 2.76, 95% CI = 1.28-5.96 (P = 0.010)), while adding salt at the table correlated with sex (men) (OR = 4.47, 95% CI = 1.21-16.57 (P = 0.025)), age (54-59) (OR = 0.05 95% CI = 0.01-0.39, (P = 0.005)), and knowledge (general) (OR = 1.06, 95% CI = 0.99-1.13 (P = 0.05)).ConclusionThe different pattern of salt intake was observed between men and women. In general, the amount of salt taken by hypertensive patients is higher than recommended allowances. Both men and women add extra amount of salt to food, women when preparing food and men at the table. Salt intake level both during preparing and eating food may be associated with occupation (unemployed), blood pressure level (systolic/diastolic ≥140/90), sex (men), age (54-59), and also patient knowledge (general).
| S-EPMC7168708 | biostudies-literature
Project description:BackgroundAlthough a number of medicines are available for the management of hypertension, the organ damage induced by hypertension is not resolved. The aim of this study was to investigate the protection of ginsenoside Rg1 (Rg1) against vascular remodeling and organ damage in spontaneously hypertensive rats (SHR).MethodsMale SHR were treated with 5, 10 or 20 mg/kg Rg1 through intraperitoneal injection per day for 1 month. SHR or Wistar-Kyoto rats (WKY) receiving vehicle (saline) was used as control. Blood pressure detection and pathological stain, transmission electron microscope, immunohistochemical assay were used to elucidate the protection of Rg1.ResultsBlood pressures were not different between control SHR rats and Rg1 treated SHR rats, but Rg1 improved the aortic outward remodeling by lowering the lumen diameter and reducing the media thickness according the histopathological and ultrastructural detections. Rg1 also protected the retinal vessels against inward remodeling detected by immunohistochemical assay. Furthermore, Rg1 attenuated the target heart and kidney damage with improvement on cardiac and glomerular structure.ConclusionsThese results suggested that Rg1 held beneficial effects on vascular structure and further protected against the organ-damage induced by hypertension. These findings also paved a novel and promising approach to the treatment of hypertensive complications.
| S-EPMC3453499 | biostudies-literature
Project description:Objective: The aim of this study was to confirm the potential role of testosterone in hypertension and target organ damage (TOD) in hypertensive postmenopausal women. Methods: A matched group study was conducted. One hundred sixty-one hypertensive postmenopausal women between 45 and 65 years of age were enrolled as group 1. Another 161 age-matched hypertensive men were enrolled as group 2. Ambulatory blood pressure monitoring, echocardiographic imaging, vascular function, sex hormones and clinical characteristics were evaluated. Quantitative data were analyzed using independent Student's t-test and multiple regression analysis. Results: The mean and load level of blood pressure were lower in women than in men (P<0.05), except for the mean level and load of the nocturnal systolic blood pressure (SBP) (123.77±15.72 mmHg vs 126.35±15.64 mmHg, and 50.43±30.31% vs 55.35±28.51%, P>0.05). However, the carotid-femoral pulse wave velocity (cf-PWV) in women was higher than that in men (9.68±2.23 m/s vs 8.03±2.82 m/s, P<0.05). The ratio of the early diastolic mitral peak flow velocity to early diastolic mitral annular velocity (E/Em) was obviously impaired (13.06±3.53 vs 12.05±3.68, P<0.05) in women. Furthermore, in women, a positive correlation was found between testosterone and cf-PWV (γ=0.157, P=0.046), and Cf-PWV was positively related to the mean level of nighttime SBP (γ=0.210, P=0.008). Moreover, nocturnal SBP was a risk factor for E/Em (γ=0.156, P=0.048, P<0.05). Conclusion: Testosterone may play a role in the correlation between hypertension and TOD in hypertensive postmenopausal women. Clinical Trial number: This research study was registered under the ClinicalTrials.gov PRS Website (NCT03451747).
| S-EPMC6501555 | biostudies-literature
Project description:Early onset hypertension confers increased risk for cardiovascular mortality in the community. Whether early onset hypertension also promotes the development of target end-organ damage (TOD), even by midlife, has remained unknown. We studied 2680 middle-aged CARDIA study (Coronary Artery Risk Development in Young Adults) Study participants (mean age 50±4 years, 57% women) who underwent up to 8 serial blood pressure measurements between 1985 and 2011 (age range at baseline 18-30 years) in addition to assessments of echocardiographic left ventricular hypertrophy, coronary calcification, albuminuria, and diastolic dysfunction in 2010 to 2011. Age of hypertension onset was defined as the age at first of 2 consecutively attended examinations with blood pressure ≥140/90 mm Hg or use of antihypertensive medication. Participants were divided in groups by hypertension onset age (<35 years, 35-44 years, ≥45 years, or no hypertension). While adjusting for TOD risk factors, including systolic blood pressure, we used logistic regression to calculate odds ratios for cases (participants with TOD) versus controls (participants without TOD) to examine the relation of hypertension onset age and hypertensive TOD. Compared with normotensive individuals, hypertension onset at age <35 years was related to odds ratios of 2.29 (95% CI, 1.36-3.86), 2.94 (95% CI, 1.57-5.49), 1.12 (95% CI, 0.55-2.29), and 2.06 (95% CI, 1.04-4.05) for left ventricular hypertrophy, coronary calcification, albuminuria, and diastolic dysfunction, respectively. In contrast, hypertension onset at age ≥45 years was not related to increased odds of TOD. Our findings emphasize the importance of assessing age of hypertension onset in hypertensive patients to identify high-risk individuals for preventing hypertensive complications.
| S-EPMC6938569 | biostudies-literature
Project description:1. Cyclic guanosine monophosphate (cyclic GMP)-mediated mechanism plays an important role in vasodilatation and blood pressure regulation. We investigated the effects of high salt intake on the nitric oxide (NO) - cyclic GMP signal transduction pathway regulating relaxation in aortas of spontaneously hypertensive rats (SHR). 2. Four-week-old SHR and normotensive Wistar-Kyoto rats (WKY) received a normal salt diet (0.3% NaCl) or a high salt diet (8% NaCl) for 4 weeks. 3. In aortic rings from SHR, endothelium-dependent relaxations in response to acetylcholine (ACh), adenosine diphosphate (ADP) and calcium ionophore A23187 were significantly impaired by the high salt intake. The endothelium-independent relaxations in response to sodium nitroprusside (SNP) and nitroglycerin were also impaired, but that to 8-bromo-cyclic GMP remained unchanged. On the other hand, high salt diet had no significant effects on the relaxations of aortic rings from WKY. 4. In aortas from SHR, the release of NO stimulated by ACh was significantly enhanced, whereas the production of cyclic GMP induced by either ACh or SNP was decreased by the high salt intake. 5. Western blot analysis showed that the protein level of endothelial NO synthase (eNOS) was slightly increased, whereas that of soluble guanylate cyclase (sGC) was dramatically reduced by the high salt intake. 6. These results indicate that in SHR, excessive dietary salt can result in downregulation of sGC followed by decreased cyclic GMP production, which leads to impairment of vascular relaxation in responses to NO. It is notable that chronic high salt intake impairs the sGC/cyclic GMP pathway but not the eNOS/NO pathway.
| S-EPMC1572996 | biostudies-other