Journal of Hypertension: Open Access

Objective: We investigated the effects of angiotensin II (Ang II) type 1 (AT1) receptor blocker (ARB) olmesartan on impaired endothelial progenitor cells (EPCs) and renal degeneration through angiotensin converting enzyme 2 (ACE2)/ Ang-(1–7)/Mas receptor (MasR) axis in salt-loaded spontaneously hypertensive rats (SHRs).

Methods: Wistar-Kyoto/Izm (WKY) rats and SHR/Izm were salt-loaded. SHRs were treated with vehicle, hydralazine, olmesartan, and olmesartan plus MasR antagonist A779 for 2 weeks. Peripheral blood mononuclear cells were isolated and subjected to flow cytometric analysis to determine the number of circulating EPCs. To evaluate the mechanisms of effects of olmesartan on renal degeneration, we investigated morphological changes and expression of ACE1, ACE2, MasR, VEGF, eNOS, NAD(P)H oxidases, HIF-1α, CTGF and TGF-β1 proteins in the kidneys.

Results: In SHRs, olmesartan was found to significantly increase EPC number and improve glomerulosclerosis; effects which were blunted with MasR antagonist A779. Expressions of CD34, P-eNOS, ACE2 and MasR proteins were significantly lower in SHR kidneys than in WKY rats. Olmesartan was found to significantly upregulate decreased expression of these proteins, this was blunted with A779. Expressions of VEGF, ACE1, NAD(P)H oxidases, HIF- 1α, CTGF and TGF-β1 were significantly higher in the kidneys of SHRs than in WKY rats. Olmesartan significantly downregulated their increased expression, an effect which was also blunted with A779.

Conclusion: Olmesartan improved impaired EPC formation and renal degeneration through the ACE2/Ang-(1– 7)/MasR axis in salt-loaded SHRs, suggesting that the ACE2/Ang-(1–7)/MasR axis represents a potential target for hypertension.

Resistant hypertension is the term used for patients who are tolerant to a maximum of three doses of antihypertensive drugs, where one of them is a diuretic. Resistant hypertension also applies to patients who are unable to reach the target blood pressure. Patients with resistant hypertension are at a higher risk of cardiovascular morbidity and mortality than those whose hypertension is controlled well.

Evidence suggests that baroreceptors play an important role in a long-term blood pressure regulation. Previous studies in animals and humans have demonstrated safe and effective blood pressure decrease with chronic electrical stimulation of the carotid sinus. Electrical baroreflex stimulation appears safe and effective and may be a useful adjunct to medical treatment in patients with resistant hypertension. This review discusses the evolution and patophysiological basis of carotid baroreceptor stimulation as well as the current data available from ongoing trials.

Aims: Renal denervation using the point-by-point application of radiofrequency (RF) energy delivered by the firstgeneration Symplicity system is effective in lowering office blood pressure however it is time-consuming. The Vessix Renal Denervation System with eight balloon-mounted bipolar electrodes shortens and simplifies the procedure. This has been the first in-human case examining the efficiency of reducing blood pressure and also the effect of RF energy in case of renal denervation on the normal functioning of pacemaker and the tolerability of the procedure in case of a patient living with pacemaker.

Materials and methods: The diabetic patient with a coronary artery disease had a baseline office systolic blood pressure ≥ 150 mmHg and took four antihypertensive medications. She had a Biotronik Talos S pacemaker with a unipolar Biotronik PX 60 UP lead because of sick sinus syndrome however she was not dependent on pacemaker. We applied 30 sec. long RF treatments in the renal artery two times.

Results: The patients baseline systolic BP was 185 mmHg which reduced by 30 mmHg immediately after the denervation. The lowering of blood pressure was permanent during the 24-hour and four-months supervisions, despite the fact that we carried out the intervention only on one side. The radiofrequency energy did not have an impact on the normal functioning of the pacemaker during and after the intervention. It did cause less physical and psychological burden for the patient than a longer procedure.

Study background: Albuminuria and nighttime blood pressure (BP) elevation are notable risk markers of chronic kidney disease (CKD). In non-diabetic patients with albuminuria, the effect of albuminuria on nocturnal BP and other risk factors that may disrupt circadian BP rhythm remain unclear. The aim of this study was to evaluate the relationship among albuminuria, serum albumin level and 24-hour BP rhythm in non-diabetic subjects.

Methods: This prospective study enrolled 778 subjects (aged 20-80 years, estimated glomerular filtration rate ≥ 60 mL/min/1.73 m2). Main outcome measure was sleeping/waking mean BP (MBP) ratio as an indicator of circadian BP rhythm. First, a cross-sectional study was performed in all individuals showing no proteinuria. Second, a study was done in subjects never treated for hypertension (hypertensive-naïve) stratified by urinary albumin excretion. Third, an intervention study was conducted in patients with massive albuminuria and hypoalbuminemia to examine circadian BP changes induced by treatment.

Results: In 441 subjects without proteinuria, multivariate regression analyses identified serum albumin, cholesterol level and circadian sympathovagal rhythm as independent predictors of sleeping/waking MBP ratio. Among hypertensivenaïve non-diabetic subjects (n=231), sleeping/waking MBP ratio increased with increasing albuminuria and decreasing serum albumin. Of 37 non-diabetic nephrotic patients who underwent treatment, 25 with serum albumin level increased to >3 g/dL showed a significant decrease (P=0.026) in sleeping/waking MBP ratio after treatment, whereas 13 with urinary albumin/creatinine lowered to <300 mg/g showed no significant difference (P=0.191).

Conclusions: This study identified low serum albumin as an independent predictor of loss of nocturnal BP decline, which was also associated with massive albuminuria. Furthermore, sleeping/waking MBP ratio was improved after hyperalbuminuria and hypoalbuminemia were reversed by treatment. These findings suggest that low serum albumin level and massive albuminuria are risk markers of disrupted circadian BP rhythm in non-diabetic early stage CKD.

Objective: The objective of this study was to compare serum calcium, magnesium and Parathyroid hormone in preeclamptic women and normal pregnant females.

Materials and Methods: 32 pregnant women, preeclamptic n=16 and healthy pregnant control group n=16 with same ages and period of gestation included in present study. Serum calcium, Magnesium and Parathyroid Hormone were done by standard methods. Data are presented as mean ± SEM. P value < 0.01 was considered statistically significant.

Results: Serum calcium (7.02 ± 0.99 vs. 9.34 ± 0.57) and serum magnesium (1.3 ± 0.34 vs1.88 ± 0.16) was significantly lower in preeclamptic women than normal healthy controls. PTH (Intact) concentration was not changed as compare to normal control (24.07 ± 4.98 vs. 23.86 ± 3.30).

Conclusion: Decreased levels of serum Calcium and serum Magnesium found in our study confirms there strong relation with preeclampsia. Calcium and magnesium supplement can be used in pregnant women for the prevention of preeclampsia.

Masked hypertension refers to a condition with normal office and elevated home or ambulatory BP without antihypertensive medication. It is a common phenomenon in a general population with a prevalence of 8-17%. However, the persistence of masked hypertension is limited, and agreement between home and ambulatory BP is only moderate. Different definitions for masked hypertension are still used, for example, elevated 24-hour, daytime, working or nighttime BP. Masked hypertension has been associated with high-normal office BP, obesity, male gender, and metabolic or lifestyle risk factors but these findings have not always been consistent. Masked hypertension has also been related to target organ damage, most commonly left ventricular hypertrophy. The cardiovascular risk associated with masked hypertension in a general population is still controversial and may, in part, be related to other concomitant cardiovascular risk factors. There is no evidence on the treatment and cost-effectiveness of masked hypertension. Implementation of out-of-office BP measurement and identification of masked hypertension in clinical practice requires interaction with general practitioners. Further studies need to map and bridge the gaps between experts´ recommendations and needs of general practitioners.

Background: The ADD1 Gly460Trp polymorphism has been linked to essential hypertension (EH) in multiple populations, but the results were inconsistent. The goal of our study is to investigate the contribution of ADD1 Gly460Trp polymorphism and environmental factors to the risk of EH.

Methods: We conducted a case-control study including 1020 hypertensive cases and 1020 controls, and the gender and age were well matched between hypertensive and control groups. Blood samples and participants information were also collected. Using the melting temperature shift technology, the ADD1 Gly460Trp polymorphism was genotyped among all subjects. Multifactor dimensionality reduction (MDR) was used to identify the interactions among the ADD1 Gly460Trp polymorphism and the nongenetic factors.

Results: Our results showed that body mass index (BMI), total cholesterol, triglycerides, and drinking were significantly associated with EH (P<0.05). In addition, the Gly460Trp polymorphism was found significantly associated with hypertension at allelic level (P<0.01; OR=0.85; 95%CI=0.75-0.96). A breakdown association analysis by gender showed the Gly460Trp polymorphism was associated with EH only in female (P<0.01; OR=0.79; 95%CI=0.68- 0.92). MDR analysis indicated that there was an interaction among BMI, high density lipoprotein, drinking, and rs4961 involved in the risk of EH.

Conclusion: The present study indicated the Gly460Trp polymorphism was associated with EH in female Han Chinese, which might contribute to EH via interactions with non-genetic factors.