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To explore the relationship between serum folic acid (FA) or Vitamin B12 (VB12) and elevated BP in children and adolescents. Both a nested case control and a cohort study were designed to explore the relationship between serum folic acid (FA) or Vitamin B12 (VB12) and elevated blood pressure (BP). All the included participants were from primary school. A total of 326 subjects (116:210) in nested case control were from an established cohort. And 270 participants without hypertension at baseline and followed in 2019 in cohort. FA and VB12 levels were lower in the elevated BP group than in the control group, and homocysteine level was higher than that in the control group. In the elevated BP group, overweight/obese children had lower FA than overweight/obese children in the normal BP group. FA was positively correlated with high-density lipoprotein (HDL) and Apo lipoprotein A (APOA), but negatively correlated with triglyceride (TG). FA was significantly correlated with elevated BP in children and adolescents (β = -0.353, P = 0.032), after adjusting VB12, and homocysteine (HCY), and the interaction effect of FA*HCY was significant. Both systolic and diastolic BP levels were statistically lower in the FA high exposure group than in the FA low exposure group in the cohort study. This study found that FA and vitamin B12 deficiency in childhood was correlated with elevated BP levels, which may affect BP by regulating lipid levels, and confirmed the importance of maintaining high levels of FA and vitamin B12 in childhood either by diet or supplementation., Competing Interests: Competing interests: The authors declare no competing interests. Ethics approval and consent to participate: The Institutional Review Board at the Children’s Hospital of Chongqing Medical University gave its approval for the study. Informed consent to participate in this study was provided by all of the children and their parents/guardians. Consent for publication: All authors critically reviewed and approved the publication of the final paper., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

MicroRNAs are key molecules involved in the regulation of endothelial function. They are important risk factors and biomarkers for the development of hypertension related to endothelial dysfunction. However, the gene expression patterns associated with hypertension development related to endothelial dysfunction have not been fully elucidated. We conducted a case-control study of 65 patients with essential hypertension (EH) and 61 controls without EH. Plasma levels of miR-122 and its target protein high-affinity cationic amino acid transporter 1 (CAT-1) were measured by qRT-PCR and ELISA, respectively. miR-122 expression in plasma of patients with EH was significantly higher than that of the control group (p = 0.001), while CAT-1 expression in patients with EH was significantly lower than that in the control group (p = 0.018). miR-122 expression in plasma of young patients with EH was significantly higher than that in young people without EH (p = 0.0004), and CAT-1 expression in plasma of young patients with EH was also significantly lower than that of the control group (p = 0.002). CAT-1 expression in the plasma of young participants was significantly higher than that of individuals aged ≥40 years (p = 0.003), whereas miR-122 expression was significantly lower (p = 0.001). We showed that among patients with EH, the high expression of miR-122 contributed to endothelial dysfunction by suppressing the expression of the CAT-1 protein, which led to a decrease in CAT-1 expression in plasma. Therefore, high expression of miR-122 appears to be a risk factor for endothelial dysfunction in EH, especially in younger patients.

We investigated changes in blood pressure (BP) and metabolic adverse effects, especially elevation of uric acid (UA), after treatment with a thiazide-like diuretic (TD) in patients with essential hypertension. Furthermore, the role of genetic factors in the elevation of UA by TD was assessed by a 500 K SNP DNA microarray. The subjects included 126 hypertensive patients (57 women and 69 men, mean age 59 ± 12 years) who registered for the GEANE (Gene Evaluation for ANtihypertensive Effects) study. After one month of the nontreatment period, TD, indapamide, angiotensin II receptor antagonist valsartan, and Ca channel blocker amlodipine were administered to all patients for 3 months each in a randomized crossover manner. BP, renal function, serum UA level, and electrolytes were measured at baseline and at the end of each treatment period. Single nucleotide polymorphisms (SNPs) associated with UA elevation after treatment with indapamide were investigated by a genome-wide association study (GWAS). Indapamide significantly decreased both office and home BP levels. Treatment with indapamide also significantly reduced the estimated glomerular filtration rate and serum potassium and increased serum UA. Patients whose UA level increased more than 1 mg/dl showed significantly higher baseline office SBP and plasma glucose and showed greater decline in renal function compared with those who showed less UA increase (<1 mg/dl). Some SNPs strongly associated with an increase in UA after treatment with indapamide were identified. This study is the first report on SNPs associated with UA elevation after TD treatment. This information may be useful for the prevention of adverse effects after treatment with TD.

Plasma markers have been continuously advocated as pointers to estimate the long-term risk of cardiovascular disease in the general population. We examined the relationship between plasma high-sensitivity C-reactive protein (hs-CRP), homocysteine (Hcy), high-sensitivity cardiac troponin T (hs-cTnT), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), 25-Hydroxyvitamin D (25OHD), glycosylated hemoglobin A1c (HbA1c), and serum uric acid (SUA) levels and hypertension in middle and old aged population. A total of 2624 Chinese (62.02 ± 5.73 years old) were recruited into a population-based, cross-sectional study. Plasma hs-CRP, Hcy, HbA1c, and SUA levels were significantly higher in the hypertension group compared with control in the entire population and men (P = 0.05 for all). We observed a positive association between the highest quartiles of Hcy, NT-proBNP, HBA1c concentrations, and the prevalence of hypertension, OR (95% CI) = 1.48 (1.16-1.90), 1.62 (1.27-2.07) and 1.94 (1.49-2.52), respectively. The multivariable-adjusted OR of hypertension for the fourth versus the first quartile of homocysteine were 2.00 and 1.39 in men and women, respectively. In conclusion, our study found an independent and robust association between elevated Hcy, NT-ProBNP, and HBA1c levels and prevalence of hypertension in the middle-aged and elderly Chinese population. A follow-up study is necessary to endorse the observed association.

The aim is to investigate the association between alterations in the serum potassium (K+) concentration and sleep architecture parameters in essential hypertensives. Two hundred ninety-two hypertensives undergoing polysomnography and providing blood samples were recruited. The sleep architecture was composed of sleep stages 1 (N1), 2 (N2), 3 (N3), 4 (N4) and REM. The light sleep stage (LST) was composed of N1 + N2, and the deep sleep stage (DST) was composed of N3 + N4. The potentialrelationships between electrolytes and sleep parameters were determined via univariate and multivariate analyses. The subjects were divided into two groups via the serum K + median (3.86 mmol/L). The K +  < 3.86 mmol/L group showed significantly decreased N1 (7.10 ± 4.55% vs 8.61 ± 5.23%, p = 0.002), LST (71.48 ± 11.33% vs 75.92 ± 17.08%, p = 0.013), and periodic leg movement during sleep related to microarousals (MA) /arousal (PLMS-A) [4 (1~10) vs 8 (3~15)/night, p < 0.001] and increased REM (17.38 ± 6.43% vs 15.37 ± 6.18%, p = 0.007) compared to the K +  ≥ 3.86 mmol/L group. A subdivided analysis by gender showed that these changes were more statistically significant in men than in women. Significant positive correlations were identified between K + and N1 (r = 0.169, p = 0 . 004), as well as PLMS-A (r = 0.222, p < 0.001) in subjects. Compared to women, a significantly strong correlation was identified between K+ and REM sleep in men (r = 0.158, p = 0.028 vs. r = 0.078, p = 0.442). Multiple linear regression analysis indicated that K+ is significantly associated with N1 in all subjects (p = 0.03) and with REM in men (p = 0.008), even after adjusting for confounders. Decreased K+ may disturb the homeostasis of the sleep architecture, and gender may interfere with their links in the hypertensive population.

This study was conducted to explore interactions in the association of the kininogen (KNG1) Ile197Met polymorphism and gender with plasma concentrations of irbesartan in Chinese patients with essential hypertension. A total of 1100 subjects with essential hypertension received a daily oral dose of 150 mg irbesartan for twenty-eight consecutive days. High-performance liquid chromatography-fluorescence (HPLC) was used to detect plasma irbesartan concentrations on day 28. The KNG1 Ile197Met gene polymorphism was determined using high-throughput TaqMan technology. The frequency distribution of KNG1 Ile197Met genotype conformed to the Hardy-Weinberg equilibrium. After 28 days of treatment, patients with the GG genotype had significantly lower irbesartan concentrations (P = 0.033) compared to homozygous TT genotype carriers. After stratifying by gender, male G allele carriers had significantly lower irbesartan concentrations (GG, P = 0.015; TG, P = 0.015, respectively) relative to TT genotype after adjusting for age, region, body mass index (BMI), smoking, and alcohol consumption. However, there was no significant difference in female subjects. A further test for a multiplicative interaction between the KNG1 Ile197Met polymorphism and gender in association with ln-plasma irbesartan concentrations in a multiple linear regression model was also significant (P for interaction = 0.033). This is the first study to suggest that gender may influence the association of the Ile197Met variant of KNG1 with ln-plasma irbesartan concentration. This finding may indicate that the interaction of gender and the KNG1 Ile197Met gene polymorphism can influence plasma trough irbesartan concentrations, which may contribute to a better development of personalized hypertensive treatment in Chinese patients.

This study aimed to examine the relationship between the ratio of monocyte frequency to high-density lipoprotein (HDL) cholesterol level (the monocyte/HDL ratio (MHR)) and asymptomatic organ damage (AOD) in primary hypertension (PHT). A total of 366 participants were enrolled in the study, including 275 cases currently being followed up after a diagnosis of PHT in our clinic and 91 healthy volunteers. The MHR was higher in patients with PHT than in individuals in the control group. In the PHT group, the MHR was higher in patients with AOD (AOD+) than in patients without AOD (AOD-). In the correlation analyses performed in the PHT group, there were positive correlations between the MHR and the following AOD indicators: carotid intima media thickness, left ventricular mass index, urinary protein levels and urinary albumin levels. In a multivariate linear regression analysis, the MHR was found to be an independent risk factor associated with these indicators of AOD. In conclusion, our study shows that MHR is associated with AOD in patients with PHT.

Despite the easy and reliable methods of blood pressure measurement, the screening of essential hypertension (EH) is usually ignored due to delayed onset of symptoms. A probe into the biochemical changes in hypertension would serve as a welcome asset to provide insight into the mechanistic aspects of EH. Filtered serum samples from 64 EH patients and 59 healthy controls (HC) were analysed using 800 MHz nuclear magnetic resonance (NMR) spectroscopy. Application of principal component analysis (PCA) and orthogonal partial least-squares discriminant analysis (OPLS-DA) following receiver operating characteristic (ROC) curve of NMR data reveals significantly perturbed metabolites: alanine, arginine, methionine, pyruvate, adenine, and uracil. This set of metabolites correctly classified 99% of cases from HC and also showed excellent correlation in both isolated elevated diastolic blood pressure (DBP) cases and combined elevated systolic-diastolic blood pressure cases. Proton NMR metabolomics of EH may prove helpful in defining associated biomarkers and serve as an alternate diagnostic tool with judicious clinical assessment.

MicroRNAs (miRs) are key posttranscriptional regulators of gene expression in all eukaryotic cells and have a vital role in the evolution of hypertension and cardiovascular remodelling and, therefore, have emerged as potential biomarkers for cardiovascular disease. We assessed 240 participants, including 60 healthy volunteers with normal carotid intima-media thickness (nCIMT), 60 healthy volunteers with increased CIMT (iCIMT), 60 hypertensive patients with nCIMT and 60 hypertensive patients with iCIMT. All patients underwent measurements of CIMT, carotid-femoral pulse wave velocity (cfPWV) and ambulatory blood pressure (BP) monitoring. Plasma miR-92a expression was quantified by real-time reverse transcription PCR. Correlations between miR-92a expression and BP parameters, CIMT and cfPWV were assessed using the Spearman correlation coefficient. We observed the lowest miR-92a expression (24.59±1.30 vs 27.76±2.13 vs 29.29±1.89 vs 33.76±2.08; P<0.001) in healthy controls with nCIMT, followed by healthy controls with iCIMT, then hypertensive patients with nCIMT and the highest expression in hypertensive patients with iCIMT. Additionally, MiR-92a levels showed a significant positive correlation with 24-h mean systolic BP (r=0.807, P<0.001), 24-h mean diastolic BP (r=0.649, P<0.001), 24-h mean pulse pressure (PP) (r=0.697, P<0.001), 24-h daytime PP (r=0.654, P<0.001), 24-h nighttime PP (r=0.573, P<0.001), CIMT (r=0.571, P<0.001) and cfPWV (r=0.601, P<0.001). Our data present significant evidence that circulating miR-92a represents a potential noninvasive atherosclerosis marker in essential hypertensive patients.

Inflammation has been shown to play a pivotal role in the pathogenesis and development of hypertensive vascular injury. Neopterin is a novel marker of immune activation produced mainly by activated macrophages. Few data are available to show the association between neopterin and vascular function in hypertension. The present study was designed to investigate the relationship between neopterin levels related to arterial stiffness and endothelial function in patients with hypertension, and their changes after blood pressure-lowering treatment. Twenty-four hypertensive patients and 30 age- and gender-matched healthy volunteers were recruited. Plasma neopterin levels were higher in hypertensive patients compared with their counterparts (log-neopterin: 0.77±0.18 versus 0.61±0.16, P=0.003). Increased neopterin levels were correlated with increased brachial-ankle pulse wave velocity (baPWV; control: r=0.659, P<0.001; hypertension: r=0.487, P=0.021), and inversely associated with impaired brachial flow-mediated dilation (FMD; control: r=-0.735, P<0.001; hypertension: r=-0.557, P=0.005). Fifteen hypertensives received 3 months of standard antihypertensive treatment. Three months later, their plasma neopterin levels decreased (log-neopterin: 0.63±0.17 versus 0.50±0.19, P=0.001), whereas arterial elasticity (baPWV: 1764±101 versus 1685±96 cm s(-1), P=0.272) and endothelial function (FMD: 5.92±1.43% versus 7.73±1.31%, P<0.05) were improved. The decline in neopterin levels was linearly correlated with baPWV decrease (r=0.800, P<0.001), FMD improvement (r=0.670, P=0.006) and blood pressure reduction (r=0.548, P=0.042). Our present study demonstrated for the first time that neopterin is closely correlated with vascular dysfunctions, and measurement of plasma neopterin levels might be used as a surrogate biomarker for the clinical evaluation of vascular damage and risk stratification of future atherosclerotic cardiovascular disease in patients with hypertension.

The critical role of metabolic abnormality in hypertension is increasingly recognized, but its biomarkers are not clearly identified. In this study, 47 chemical compounds recorded by literature were employed as target metabolites of essential hypertension (EH). We detected their content in the plasma of EH patients and healthy subjects by using the Multiple Reaction Monitoring-Mass Spectrometry (MRM-MS). After screening the most altered compounds, acupuncture was used to treat patients for 3 months and these plasma metabolites were tested again. The results showed that oleic acid (OA) and myoinositol (MI) were the most important differential metabolites between the hypertensive plasma and the healthy plasma. They were also closely correlated with 24-hour blood pressure and nocturnal dipping. Moreover, plasma OA and MI could be restored to normal levels by acupuncture, accompanying with reduction of 24-hour systolic and diastolic blood pressure [from 145.10 ± 9.28 mm Hg to 140.70 ± 9.59 mm Hg (P < 0.0001), and 88.35 ± 7.92 mm Hg to 85.86 ± 7.95 mm Hg (P = 0.0024), respectively] and improvement of circadian blood pressure rhythm. This study demonstrated that plasma OA and MI were potential hypertension biomarkers and they could be used to preliminarily assess the treating effects such as acupuncture.