Journal of Hypertension: Open Access

Objective: We estimated the daily sodium intake using a spot urine method in hypertensive patients, and investigated the differences in the pressure-natriuresis relationship depending on the type of medications and the involvement of renal function in this relationship.

Methods: This study included 356 spot urine samples of hypertensive patients at our cardiology outpatient clinic. Daily sodium intake was estimated by the spot urine tests at the time of study enrolment. We examined the difference in the relationships among estimated daily sodium intake, mean blood pressure (mBP), and estimated glomerular filtration rate (eGFR) with each medication.

Results: In multivariate analysis, the eGFR and mBP were significantly associated with estimated daily sodium intake. The slope of the pressure-natriuresis relationship was steeper in patients treated with renin-angiotensin system inhibitors (RAS-I) plus diuretics, and lower in patients treated with RAS-I plus calcium-channel blockers (CCB) than in those treated with CCB or who were not treated. eGFR was higher in patients with higher daily sodium intake than in those with lower daily sodium intake in association with higher mBP, except for patients treated with CCB alone.

Conclusions: Estimated daily sodium intake in hypertensive patients was positively correlated with eGFR and mBP. The slope of the pressure-natriuresis relationship curve was different depending on the class of medication. In hypertensive patients with higher sodium intake, the relationship between mBP and eGFR may be important when selecting the type of medication.

Background: Prevalence of orthostatic hypotension (OH) has been investigated in many studies, mainly on selected samples of subjects. We aimed to assess the prevalence of OH and its association with incidence of adverse events among older medical inpatients.

Methods: OH was evaluated according to current guidelines at admission and at discharge among older medical inpatients admitted to a Geriatric acute ward of an university-teaching hospital. A comprehensive clinical (CIRS, Cumulative Illness Rating Scale), functional (ADL, Activities of Daily Living; IADL, Instrumental Activities of Daily Living Scale, TUG, Timed Up and Go) and cognitive (SPMSQ, Short Portable Mental Status Questionnaire) evaluation was performed. Length of stay-in and adverse events (death, institutionalization, falls, syncope, posttraumatic fractures, cardiovascular events) were evaluated at discharge and at 6 months.

Results: Among 343 patients admitted, 195 (mean age 80.1 ± 7.2) were enrolled. Prevalence of OH at admission was 52.3%; patients with OH had higher systolic and diastolic blood pressure values (p=0.001 both) and lower heart rate (p=0.02) than patients without OH. Although several conditions were associated with presence of OH, only history of neurological and coronary artery disease were slightly independently associated with OH (p=0.03 and p=0.02, respectively). Prevalence of OH at discharge was 49%. OH was not significantly associated with any adverse event, nor during the hospital stay nor after discharge.

Conclusion: OH is extremely common among elderly inpatients, but it was not associated with adverse events. Our results question the utility of routinely screening older medical inpatients for OH.

The epidemiology study was done to evaluate the prevalence and contributing factors for hypertension in western Indian. Total 3629 patients eligible for study; overall prevalence of hypertension was 26% and approximately 10% in younger (<40 yrs) age group. The obesity and sedentary life style plays important role in development of hypertension in overall population while family history of hypertension and obesity influence in younger.

Objective: The study investigated the impact of renal sympathetic denervation on office blood pressure and ambulatory blood pressure monitoring in patients with resistant hypertension. We evaluated whether a decrease in blood pressure may improve local carotid stiffness and parameters of wave intensity.

Methods: Renal sympathetic denervation was performed in 17 patients (age 55 ± 9 years) with true resistant hypertension. Measurements of carotid stiffness and wave intensity were performed using ultrasound combined with echo-tracking.

Results: We found significantly improved office systolic blood pressure changes 1 month (p=0.023) and together with pulse pressure changes at the 6 month follow up (p=0.041; p=0.016). Changes in systolic blood pressure during the daytime were significantly decreased at 1 month and diastolic blood pressure changes during the daytime were significantly reduced at 1 and 3 months. Stiffness parameters beta stiffness and pressure-strain elastic modulus were significantly reduced (p=0.04; p=0.03) and arterial compliance was increased (p=0.03), especially 1 and 3 months. The changes in negative area were significantly reduced after 1 month (p=0.041) and the ejection period was significantly increased at the 6 month follow-up (p=0.011). According to linear regression analysis systolic blood pressure correlated positively with the beta stiffness, pressure-strain elastic modulus, pulse wave velocity, and negatively with arterial compliance.

Conclusions: We found significantly lower office blood pressure as well as blood pressure from ambulatory blood pressure monitoring in patients with resistant hypertension 6 months after renal sympathetic denervation. The decrease in blood pressure was followed by improvement of carotid stiffness and wave intensity. That may be reflected in enhancement of ventricular-arterial coupling.

Background: In this study, we aimed to determine PTX3 levels in hypertensive patients with nephropathy, retinopathy and stroke.

Methods: This study is considering totally 135 patients including normotensives and newly diagnosed hypertensive and hypertensive with nephropathy, retinopathy and stroke. Blood samples were extracted to perform biochemical tests and PTX3 levels.

Results: It is observed that PTX3 levels in the normotensive patients, isolated hypertensive patients and hypertensive patients have complication resulted with statistically differences (0.19 ± 0.15 ng/Ml, 37.15 ± 8.02 ng/Ml, 451.28 ± 244.39 ng/mL, p<0.00001). This arises from the differences between the PTX3 levels which belong the patient group has complication along with other groups and isolated hypertensive group along with normotensive group by the performed Post Hoc analyze. If the patients have complication are compared with each other, it is observed PTX3 level in the retinopathy group is statistically higher with reference to other groups (In retinopathy, neuropathy and nephropathy groups’ 710.90 ± 254.6 ng/mL, 408.14 ± 65.56 ng/mL, 253.61 ± 62.66 ng/mL, p<0.0001 respectively). It was established PTX3 levels in the complicated hypertensive patients is associated with BMI and LDL/HDL by the performed multivariate regression analysis (For BMI, LDL/HDL is respectively R square=0.085, F=5.84 and p=0.019 versus R square=0.153, F=5.61 and p=0.006).

Conclusion: It is observed in the present study that in hypertensive patients with stroke and retinopathy and nephropathy, and isolated hypertensive, PTX3 levels are elevated. It is also found BMI and LDL/HDL is associated with PTX3 levels.

Aim: Prostanoids and female sex hormones play an important role in the progression of hypertension. However, their close-related structures make simultaneous separation and analyses difficult. A method was developed to separate and analyze seventeen important bioactive compounds including nine prostanoids and eight sex hormones in a short time. By applying the method to quantify prostanoids and female sex hormones in urine samples from hypertension patients, it becomes possible to find effective biomarkers for clinical diagnosis, prevention and treatment of hypertension.

Materials and methods: A reversed phase high performance liquid chromatography is used to develop the separation method. A combination of up to nine prostanoids (PGD2, PGE2, 6-keto PGF1α, PGF2α, 11-dehydro TXB2, 8-iso PGF2α, 13,14-dihydro-15-keto PGA2, 13,14-dihydro-15-keto PGE2 and 15-deoxy Δ12,14 PGJ2) and eight female sex hormones (E1, E2, E3, progesterone, 2-OHE1, 4-OHE1, 16α-OHE1, and 2-MeOE1) are chosen as analytes. The separation is performed on Symmetry C18 4.6x250 mm column with 5 μm particle size. A UV detector is selected to determine the levels of analytes in a single 25-minute run.

Results: The method is the first we are aware of successfully demonstrating the separation of the two different groups of bioactive compounds prostanoids and female sex hormones. It has been shown to have excellent selectivity, sensitivity, and accuracy over biologically relevant concentration ranges and has been tested on urine samples from hypertension patients.

Objectives: The (pro) renin receptor (PRR) is highly expressed in the brain and is involved in the central regulation of blood pressure. However, the role of the brain PRR in regulating body fluid homeostasis in hypertension remains unclear. We hypothesized that the brain PRR knockdown modulates water intake, urine, and urinary sodium excretion in the context of angiotensin II (Ang II)-induced hypertension.

Methods and Results: Brain PRR was knocked down in non-transgenic (NT) normotensive and human reninangiotensinogen double-transgenic (RA) mice by intracerebroventricular (ICV) injection of adeno-associated virus expressing short hairpin RNA targeting the PRR (AAV-PRR-shRNA). Water and food intake, and urinary excretion were recorded using metabolic cages. At baseline, RA mice exhibited higher water intake, food intake, urine excretion, urinary sodium excretion and potassium excretion compared to NT mice. PRR knockdown in the brain significantly decreased water and food intake, and urinary potassium and sodium excretion in RA mice, but had no such effects in NT mice. PRR knock down also decreased reactive oxygen species generation and plasma Ang II concentration in RA mice.

Conclusion: PRR knockdown modulates body fluid homeostasis in hypertensive RA mice, suggesting that the brain PRR plays a role in regulating body fluid homeostasis during Ang II-dependent hypertension.

Background: Long-chain Free Fatty Acids (FFA) and long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) are related to some preeclampsia. We studied the relationship between LCHAD, carnitine palmitoyltransferase (CPT) I and II and FFA in different preeclampsia-like models.

Methods: Classic preeclampsia models with Nw-nitro-L-arginine-methyl ester (L-NA) or Lipopolysaccharide (LPS) injection, antiphospholipid syndrome model with β2 glycoprotein I (β2GPI) injection, and ApoC3 mice with abnormal fatty acid metabolism (ApoC3+NS and ApoC3+L-NA) were used. Controls were saline injected. At days 14 and 18 of pregnancy, serum FFA levels were compared and placental and hepatic LCHAD, CPT I and II mRNA and protein were detected using real-time quantitative PCR and western blot.

Results: Serum FFA levels increased significantly except in LPS, compared to controls (P<0.05). CPT I mRNA and protein increased significantly in the liver and placenta of L-NA and β2GPI and liver of ApoC3+L-NA (P<0.05). CPT II mRNA and protein increased significantly in the liver and placenta of L-NA and the liver of ApoC3+L-NA and β2GPI (P<0.05). LCHAD mRNA and protein increased significantly in the liver and placenta of ApoC3+NS, ApoC3+L-NA and β2GPI, and decreased significantly in L-NA (P<0.05). Serum FFA levels positively correlated with liver CPT I mRNA and protein in all groups (P<0.05) and negatively correlated with liver LCHAD mRNA and protein expression in all groups except in β2GPI group (P<0.05).

Conclusions: Changes and correlations in FFA levels and LCHAD, CPT I and II were different according to preeclampsia-like models. β-oxidation disorders may occur at different stages.

Background: PRKG1 plays an important role in regulating vascular smooth muscle contraction. And this gene is regarded as one of the candidate genes on salt-sensitive hypertension. The aim of this study was to investigate the effects of environmental risk factors and two SNPs and haplotypes structures of PRKG1 gene with blood salt-sensitive patients among essential hypertension.

Method: Three hundred and forty-two essential hypertensive were recruited in a case-case study, a modified Sullivan’s acute salt load method was conducted to identify the salt-sensitivity and salt-resistant. Medical history and lifestyle risk factors were obtained by questionnaire, and blood and urine specimens were collected to test the biochemical indicators. We used the Sequenom Mass ARRAY Platform for genotyping of PRKG1 gene single nucleotide polymorphisms (SNPs) (rs7897633/SNP1, rs1904694/SNP2). We applied statistical software SPSS17.0, multifactor dimensionality reduction method 1.1.0 and haploview 4.0 to do the analyses.

Results: There were 63 salt sensitivity subjects in 342 essential hypertension individuals, accounting for 18.4% of the total. Age and 24-hour urinary sodium concentration were the risk factors associated with salt-sensitive hypertension. The results of the logistic regression model showed that subjects carrying SNP1-AA genotype and SNP2-GG genotypes had 2.83-fold (95% CI: 1.21-6.63) and 3.50-fold (95% CI: 1.54-7.93) risks to have salt-sensitive hypertension, respectively. Haplotype analysis showed that haplotype CA had 0.56-fold (95% CI: 0.38-0.84) decreased risk for salt-sensitive hypertension, whereas, haplotype AG had 1.78-fold (95% CI: 1.20-2.65) increased risk for saltsensitive hypertension.

Conclusion: Age and 24-hour urinary sodium concentration are the environmental risk factors associated with salt-sensitive hypertension. Genotypes of SNP1-AA, SNP2-GG and haplotype AG of PRKG1 gene were risk factors for salt-sensitivity in essential hypertension.

In 2000 a group of authors from Ä°stanbul University CerrahpaÅŸa Medical Faculty Internal Medicine Department interesting in hypertension (HT) especially White Coat Hypertension (WCH) come together and began to study on WCH. We founded a team and act as a referral center in our faculty.

Cases with blood pressure >140-90 were referred to our clinic. We classified the cases into sustained hypertension (HT) and white coat hypertension (WCH) groups. We defined WCH as clinical hypertension and day time ambulatory blood pressure less than 135/85.

First of all we investigated if WCH were innocent. With this purpose we searched for the target organ damage with a cross sectional study and our manuscript was published (Target organ damage and change in arterial compliance). We studied the metabolic changes caused by WCH and it was also published within the same manuscript.

Since that time we have been following up these groups longitudinally to see if WCH turns to sustained HT or target organ damage and/or metabolic changes occur by the time. We are planning to report the progression of twenty years in 2020.

It has been documented that oxidative stress and endothelial dysfunction participated in the pathogenesis of sustained hypertension. As we observed white coat is not innocent due to our previous studies we aimed to see if there also exists oxidative stress and endothelial dysfunction in WCH with some serial studies using different markers such as asymmetric dimethyl arginine (ADMA) a competitive inhibitor of NO (nitric oxide), homocystein (decreasing the bioavailibity of NO), paroxanase (PON; preventing lipid oxidation), oxLDL, sLOX-1 (oxidation products of lipids and proteins) and endogenous antioxidan components. It has been observed that the majority of our studies evaluating endothelial function indicated that endothelial dysfunction is more prevalent in WCH than in NT, but it is either equal or worse in HT as compared to WCH.

Hypertension is a significant cardiovascular risk factor with multifactorial aetiology. The link between hypertension and hyperuricaemia has been noted for over a century however determining whether this link is causal and whether there is a role for management of hyperuriaemia in the context of hypertension has been more problematic. Over the past two decades research in this area has dramatically increased with development of animal models of hyperuricaemia and use of large observational cohorts. There is an emerging body of evidence that hyperuricaemia should be considered an independent risk factor for the development of essential hypertension and that further research into the management of hyperuricaemia is required.

Background and objectives: Hypertension is a prevalent condition that represents a significant morbidity and mortality. In this review, we sought to highlight the value of markers in systemic hypertension.

Design and method: we conducted a mini-review focusing on markers in hypertension, also we reviewed the JNC8-2014 and ESC/ESH-2013 recommendations in this perspective; a Pubmed search was performed accordingly.

Results: we presented and discussed markers of diagnosis and physiopathology of hypertension, markers of target organ damage and markers of blood pressure progression, with a focus on biomarkers. Genetics of hypertension is a rapidly moving field and at least 38 foci correlated to blood pressure are currently identified; the Ras homologous (Rho; RhoA, Rac1) are mainly involved in vascular smooth muscle tonus and vasoactivity; adipokines (leptin, TNF-α, IL-6, MCP-1, and IL-1) expression is marked in patients with obesity related hypertension. The baroreceptor is a marker of dysautonomia which is implicated in the pathogenesis of hypertension; miR-9 and miR-126 are markers of target organ damage in hypertensive patients. Markers of endothelial dysfunction, systemic inflammation, and oxidative stress were also discussed as causative or target organ markers in this context, with a focus on C-reactive protein and nitric oxide.

Conclusion: markers, mainly biomarkers, play an increasingly critical role in hypertension evaluation and management.

Objective: An association between the renin-angiotensin system and the pathogenesis of pregnancy-induced hypertension has been reported. The prorenin receptor was discovered in 2002, and Wanatabe et al. reported that women with plasma soluble prorenin receptor concentrations above the 75th percentile at delivery had a significantly increased risk of preeclampsia. We evaluated serum prorenin concentrations during pregnancy, and we assessed the incidence of pregnancy-induced hypertension.

Methods: We measured serum prorenin concentrations in 430 pregnant women (565 samples). Regression analysis was performed to determine the associations between the serum prorenin level and maternal/neonatal complications.

Results: The serum prorenin concentration and gestational age had a positive correlation in non-pregnancyinduced hypertension in women with singleton pregnancies (Spearman rank-correlation coefficient, -0.215: p<0.0001). The serum prorenin concentration in women with multiple pregnancies was significantly higher than that in women with singleton pregnancies (multiple linear regression analysis, p<0.0001). Low prorenin levels in the third trimester (≤20.1 percentile) were significantly associated with pregnancy-induced hypertension (adjusted odds ratio, 18.16: 95% confidential interval, 1.95-412.41: p=0.0107).

Conclusion: The serum prorenin levels during pregnancy may be adversely correlated with the prorenin receptor, and low prorenin levels during late pregnancy were significantly associated with pregnancy-induced hypertension.

Objective: To examine the phenotypes of endothelial microparticles and platelet microparticles in order to identify a sensitive endothelial microparticle biomarker for monitoring endothelial dysfunction in patients with coronary artery disease, and to examine the mechanisms underlying endothelial dysfunction.

Methods: Thirty-three coronary artery disease patients and 53 healthy subjects were recruited. The absolute numbers of endothelial microparticles and platelet microparticles were measured by flow cytometry, and the clinical characteristics of patients and healthy subjects were recorded. Spearman’s correlation analysis and multiple linear regression analysis were performed to analyse the correlation between endothelial microparticles and platelet microparticles, and between microparticles and clinical data.

Results: There was a significant difference in the number of CD31+/CD42b- endothelial microparticles and CD62E+ endotheial microparticles between patients with coronary artery diease and healthy subjects (p<0.05).

Conclusion: Both endothelial apoptosis and activation play an important role in coronary artery disease, although endothelial apoptosis plays the major role. Endothelial microparticles may be used to monitor endothelial dyfunction in patients with coronary artery disease.

Objectives: Although the Dietary Approaches to Stop Hypertension (DASH) diet lowers blood pressure in adults with hypertension, how kidney function impacts this effect is not known. We evaluated whether Estimated Glomerular Filtration Rate (eGFR) modifies the effect of the DASH diet on blood pressure, markers of mineral metabolism, and markers of kidney function.

Methods: Secondary analysis of the DASH-Sodium trial, a multicenter, randomized, controlled human feeding study that evaluated the blood pressure lowering effect of the DASH diet at three levels of sodium intake. Data from 92 participants with pre-hypertension or stage 1 hypertension during the 3450 mg /day sodium diet assignment contributed to this analysis. Stored frozen plasma and urine specimens were used to measure kidney related laboratory outcomes.

Results: Effects of the DASH diet on blood pressure, phosphorus, intact parathyroid hormone, creatinine, and albuminuria were not modified by baseline eGFR (mean 84.5 ± 18.0 ml/min/1.73 m2, range 44.1 to 138.6 ml/min/1.73 m2) or the presence of chronic kidney disease (N=13%).

Conclusions: The impact of the DASH diet on blood pressure, markers of mineral metabolism, and markers of kidney function does not appear to be modified by eGFR in this small subset of DASH-Sodium trial participants with relatively preserved kidney function. Whether greater reduction in eGFR modifies the effects of DASH on kidney related measures is yet to be determined. A larger study in individuals with more advanced kidney disease is needed to establish the efficacy and safety of the DASH diet in this patient population.