Because dementia is associated with both deterioration in the quality of life and poor prognosis, the prevention of cognitive impairment (CI) is a critical problem in public health promotion. Hypertension is a risk factor for the aggravation of CI, and the renin-angiotensin-aldosterone system (RAAS) is a key player in the increased incidence and development of hypertension. Therefore, the RAAS is considered to be a promoting factor for CI development. Conversely, recent studies have shown that lowering blood pressure with RAAS inhibitors decreases the incidence of CI, dementia and cardiovascular disease. Blood-brain barrier-penetrating RAAS inhibitors appear to have advantages in preventing cognitive decline because they can suppress the RAAS in the hippocampus, which has an important role in cognition. Thus, RAAS blockage is a notable strategy for preventing CI.Hypertension Research advance online publication, 23 May 2013; doi:10.1038/hr.2013.51.

Microalbuminuria is an early sign of nephropathy and an independent predictor of end-stage renal disease. The purpose of this study was to assess microalbuminuria prevalence and its contributing factors in Korean hypertensive patients. This cross-sectional study enrolled male and female patients of 35 years old with an essential hypertension diagnosis as made by 841 physicians in primary care clinics and 17 in general hospitals in the Republic of Korea between November 2008 and July 2009. To assess microalbuminuria prevalence, urine albumin/creatinine ratio (UACR) was measured in patients with a positive dipstick test. Of the 40 473 enrolled patients, 5713 (14.1%) had a positive dipstick test. Of 5393 patients with a positive dipstick test and valid UACR values, 2657 (6.6%) had significantly elevated UACR (30 μg mg(-1)), 2158 (5.4%) had microalbuminuria (30 μg mg(-1)UACR <300 μg mg(-1)) and 499 (1.2%) had macroalbuminuria (UACR 300 μg mg(-1)). Based on multivariate analysis, independent factors associated with elevated UACR included low adherence to antihypertensive medication (23% higher; P=0.042), poorly controlled blood pressure (BP; 38% higher for systolic BP/diastolic BP 130 mm Hg/80 mm Hg; P<0.001), obesity (47% higher for body mass index (BMI) 25.0 kg m(-2); P<0.001), age (17% lower and 58% higher for age categories 35-44 years (P=0.043) and >75 years (P<0.001), respectively) and a prior history of diabetes (151% higher; P<0.001) and kidney-related disease (71% higher; P<0.001). The prevalences of elevated UACR and microalbuminuria were 6.6% and 5.4%, respectively. Age, increased BMI, presence of comorbidities, poor medication adherence and inadequately controlled BP were independent predictors of elevated UACR after controlling for potential confounders.Hypertension Research advance online publication, 23 May 2013; doi:10.1038/hr.2013.44.

Reduced NO availability is associated with endothelial dysfunction, hypertension, insulin resistance and cardiovascular remodeling. SIRT1 upregulates eNOS activity and inhibits endothelial cell senescence, and reduced SIRT1 is related to oxidative stress and reduced NO-dependent dilation. Bartter's/Gitelman's syndromes (BS/GS) are rare diseases that feature a picture opposite to that of hypertension in that they present with normo/hypotension, reduced oxidative stress and a lack of cardiovascular remodeling, notwithstanding high levels of angiotensin II and other vasopressors, upregulation of NO system, and increased NO-dependent vasodilation (FMD), as well as increase in both endothelial progenitor cells and insulin sensitivity. To our knowledge, in BS/GS patients SIRT1 has never been evaluated. BS/GS patients' mononuclear cell SIRT1 (western blot), FMD (B-mode scan of the right brachial artery) and heme oxygenase (HO)-1 (sandwich immunoassay), a potent antioxidant protein, were compared with the levels in untreated stage 1 essential hypertensive patients (HPs) and in healthy subjects (C). SIRT1 (1.86±0.29 vs. 1.18±0.18 (HP) vs. 1.45±0.18 (C) densitometric units, P<0.0001) and HO-1 protein (9.44±3.09 vs. 3.70±1.19 (HP) vs. 5.49±1.04 (C) ng ml(-1), P<0.0001) levels were higher in BS/GS patients than in the other groups. FMD was also higher in BS/GS patients: 10.52±2.22% vs. 5.99±1.68% (HP) vs. 7.99±1.13% (C) (ANOVA: P<0.0001). A strong and significant correlation between SIRT1 and FMD was found only in BS/GS patients (r(2)=0.63, P=0.0026). Increased SIRT1 and its direct relationship with increased FMD in BS/GS patients, while strengthening the relationship among SIRT1, NO and vascular function in humans, point toward a role for reduced SIRT1 in the endothelial dysfunction of hypertension.Hypertension Research advance online publication 23 May 2013; doi:10.1038/hr.2013.48.

Inflammation has a role in the pathogenesis of atherosclerosis, which causes hypertension. Results from some studies have suggested links between periodontal disease and atherosclerosis, but links between periodontal disease and hypertension have been seldom studied. We investigated whether periodontal disease and serum antibody level were associated with hypertension. We studied 127 patients (93 men and 34 women, mean age 68±9 years) who were admitted with ischemic heart disease to our institution. A composite periodontal risk score was calculated from five periodontal vector scores. The levels of serum antibody against Porphyromonas gingivalis (Pg) were measured. Pulse pressure, mean blood pressure (BP) and pulse wave velocity were used as indices of atherosclerosis. We divided patients into two groups according to the levels of serum antibody against Pg: higher or equal to the median (high Pg antibody group) and lower than the median (low Pg antibody group).There was no difference in the use of antihypertensive agents between the two groups. The composite periodontal risk score (P=0.0003), systolic BP (P=0.030), diastolic BP (P=0.038), pulse pressure (P=0.050) and mean BP (P=0.055) were higher in the high Pg antibody group than in the low Pg antibody group. The composite periodontal risk score (r=0.320, P=0.0003), systolic BP (r=0.212, P=0.017), diastolic BP (r=0.188, P=0.035) and mean BP (r=0.225, P=0.011) correlated with the level of serum antibody against Pg, even after adjustment for age. An elevated antibody level against Pg indicates advanced periodontal disease and suggests advancement of atherosclerosis and hypertension.Hypertension Research advance online publication, 16 May 2013; doi:10.1038/hr.2013.46.

Hypertension continues to be a significant cause of morbidity and mortality, underscoring the need to better understand its early effects on the myocardium. The aim of this study is to determine the feasibility of in vivo longitudinal assessment of cardiac function, particularly diastolic function, in a mouse model of renovascular hypertension. Renovascular hypertension (RVH) was induced in 129S1/SvImJ male mice (n=9). To assess left ventricular (LV) systolic and diastolic function, M-mode echocardiography, pulsed-wave Doppler echocardiography and tissue Doppler imaging were performed at baseline, 2 and 4 weeks after the induction of renal artery stenosis. Myocardial tissue was collected to assess cellular morphology, fibrosis, extracellular matrix remodeling and inflammation ex vivo. RVH led to a significant increase in systolic blood pressure after 2 and 4 weeks (baseline: 99.26±1.09 mm Hg; 2 weeks: 140.90±7.64 mm Hg; 4 weeks: 147.52±5.91 mm Hg, P<0.05), resulting in a significant decrease in LV end-diastolic volume, associated with a significant elevation in ejection fraction and preserved cardiac output. Furthermore, the animals developed an abnormal diastolic function profile, with a shortening in the E velocity deceleration time as well as increases in the E/e' and the E/A ratio. The ex vivo analysis revealed a significant increase in myocyte size and deposition of extracellular matrix. Non-invasive high-resolution ultrasonography allowed assessment of the diastolic function profile in a small animal model of renovascular hypertension.Hypertension Research advance online publication, 16 May 2013; doi:10.1038/hr.2013.43.

Recent data suggest excess circulating aldosterone promotes cardiometabolic decline. Weight loss may lower aldosterone levels, but little longitudinal data is available in normotensive adults. We aimed to determine whether, independent of changes in sodium excretion, reductions in serum aldosterone are associated with favorable changes in obesity-related factors in normotensive overweight/obese young adults. We studied 285 overweight/obese young adult participants (body mass index25 and<40 kg m(-2), age 20-45 years) in a clinical trial examining the effects of a 1-year diet and physical activity intervention with or without sodium restriction on vascular health. Body weight, serum aldosterone, 24-h sodium and potassium excretion and obesity-related factors were measured at baseline, 6, 12 and 24 months. Weight loss was significant at 6 (7%), 12 (6%) and 24 months (4%; all P<0.0001). Decreases in aldosterone were associated with decreases in C-reactive protein, leptin, insulin, homeostasis assessment of insulin resistance, heart rate, tonic cardiac sympathovagal balance and increases in adiponectin (all P<0.05) in models adjusting for baseline age, sex, race, intervention arm, time since baseline, and sodium and potassium excretion. Weight loss and reductions in thigh intermuscular fat (intermuscular adipose tissue area; IMAT) were associated with decreases in aldosterone in the subgroup (n=98) with metabolic syndrome (MetS) at baseline (MetS × weight loss, P=0.04; MetS × change in IMAT, P=0.04). Favorable changes in obesity-related factors are associated with reductions in aldosterone in young adults with no risk factors besides excess weight, an important finding, given aldosterone's emergence as an important cardiometabolic risk factor.Hypertension Research advance online publication, 9 May 2013; doi:10.1038/hr.2013.45.