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Adverse blood pressure (BP) is a major independent risk factor for epidemic cardiovascular diseases affecting almost one third of the US adult population. This review synthesizes results from studies published over the past few years on BP differences and prevalent hypertension between US blacks and whites and their different intakes of foods (e.g., fruits, vegetables, and dairy products) and micronutrients (e.g., vitamin D, calcium, potassium, and phosphorus). Studies have consistently reported higher prevalence of adverse BP levels and hypertension and less favorable dietary intakes in blacks than in whites, but the influence of specific dietary factors on high BP risk for blacks remains unclear.

Purpose of ReviewThe purpose of this review was to summarize the current knowledge on the role of angiotensin-(1–7) [Ang-(1–7)] and alamandine in experimental hypertension and atherosclerosis.Recent FindingsThe renin-angiotensin system (RAS) is a very complex system, composed of a cascade of enzymes, peptides, and receptors, known to be involved in the pathogenesis of hypertension and atherosclerosis. Ang-(1–7), identified and characterized in 1987, and alamandine, discovered 16 years after, are the newest two main effector molecules from the RAS, protecting the vascular system against hypertension and atherosclerosis.SummaryWhile the beneficial effects of Ang-(1–7) have been widely studied in several experimental models of hypertension, much less studies were performed in experimental models of atherosclerosis. Alamandine has shown similar vascular effects to Ang-(1–7), namely, endothelial-dependent vasorelaxation mediated by nitric oxide and hypotensive effects in experimental hypertension. There are few studies on the effects of alamandine on atherosclerosis.

Hypertension is the single largest risk factor attributed to mortality in the world. Medications are the primary treatment for hypertension; however, adherence to drug regimens is low (~50 %). Low adherence may be a contributing factor leading to uncontrolled blood pressure in patients. An effective alternative or complement to medications in managing hypertension is through lifestyle modifications. Adopting a healthy diet is a valuable strategy. A recent, randomized controlled year-long trial observed impressive reductions in blood pressure in patients with hypertension consuming flaxseed daily. Therefore, attention has been garnered for flaxseed as a potentially valuable strategy for the management of hypertension. This review will highlight the recent data for flaxseed and its extracts in blood pressure regulation in both animal models and clinical trials. Insight into the proposed anti-hypertensive mechanism of flaxseed and the implications of flaxseed as a potential global anti-hypertensive therapy will be discussed.

Obstructive sleep apnea (OSA) is a prevalent sleep disorder which is characterized by recurrent upper closure with oxygen desaturation and sleep disruption. OSA increases the risk of vascular disorders in the form of stroke, myocardial infarction, congestive heart failure, and hypertension. The mechanisms underlying the vascular disorders are several and include intermittent hypoxia with release of cytokines, angiogenic inhibitors, free radicals, and adhesion molecules. During apneas, arterial blood pressure gradually rises and surges abruptly after the termination of apnea. Two thirds of patients with OSA will ultimately have diurnal hypertension. This review discusses the literature supporting the significant role of OSA in hypertension and the effect of OSA treatment on blood pressure.

The polycystic ovary syndrome (PCOS) is a hyperandrogenic disorder affecting 5–10 % of premenopausal women. These patients gather multiple cardiovascular risk factors from early ages. Hence, PCOS is currently considered a paradigm of cardiometabolic disease. Research about its pathogenesis has grown over the last years, covering from the potential fetal developmental programming to the molecular basis of adipose tissue dysfunction, insulin resistance, inflammation, oxidative stress, sympathetic hyperactivity, and endothelial dysfunction. All these abnormalities put these patients at an increased risk of vascular events. Thus, practitioners attending these women must have a broad pathophysiological knowledge of PCOS. We here review recent scientific insights about its cardiometabolic phenotype focusing on the pathogenesis of obesity, type 2 diabetes mellitus, and hypertension. We emphasize that a diagnosis of PCOS, especially if accompanied by excess weight, must be followed by a complete and periodical cardiometabolic evaluation and by the aggressive management of the abnormalities identified, with the aim of preventing future cardiovascular morbidity.

Essential hypertension (EH) and its complications have had a severe impact on public health. However, the underlying mechanisms of the pathogenesis of EH remain largely unknown. Recent investigations, predominantly in rats and mice, have provided evidence that dysregulation of distinct functions of T lymphocyte subsets is a potentially important mechanism in the pathogenesis of hypertension. We critically reviewed recent findings and propose an alternative explanation on the understanding of dysfunctional T lymphocyte subsets in the pathogenesis of hypertension. The hypothesis is that hypertensive stimuli, directly and indirectly, increase local IL-6 levels in the cardiovascular system and kidney, which may promote peripheral imbalance in the differentiation and ratio of Th17 and T regulatory cells. This results in increased IL-17 and decreased IL-10 in perivascular adipose tissue and adventitia contributing to the development of hypertension in experimental animal models. Further investigation in the field is warranted to inform new translational advances that will promote to understand the pathogenesis of EH and develop novel approaches to prevent and treat EH.

In 2010, the American College of Cardiology Foundation and American Heart Association could not recommend brachial artery percentage flow-mediated dilation (FMD%) for risk assessment of coronary artery disease (CAD) in asymptomatic adults. We aimed to scrutinise past and recently published findings regarding FMD% in this same context of clinical utility and conclude that (1) the question of whether brachial FMD% is a suitable substitute for coronary vasodilation is addressed by method agreement statistics rather than the correlation coefficients that have been reported in past studies. Also, the much-repeated view that brachial FMD% and coronary vasodilation are “closely related” is not entirely justified, even before the influence of baseline lumen diameters on this relationship is accounted for; (2) along with the specialist training and the considerable time (≥1 h) that is required for the FMD% protocol, the error in individual measurements and population reference ranges is too large for clinical decisions to be robust on individual patients; (3) many interventions that are proposed to change FMD% also change baseline artery diameter, which can bias estimates of any intervention effects on the flow-mediated response per se, and (4) the FMD% index generates spurious correlations between shear rate, artery diameter and endothelial function, which may help to explain the apparent paradoxes of FMD% being higher in obese people and lower in athletes. In conclusion, the clinical relevance of brachial artery flow-mediated dilation is unclear at present. The dependence of the chosen index, FMD%, on initial artery size has contributed to this lack of clarity.

Nitric oxide (NO), a potent vasodilator critical in maintaining vascular homeostasis, can reduce blood pressure in vivo. Loss of constitutive NO generation, for example as a result of endothelial dysfunction, occurs in many pathological conditions, including hypertension, and contributes to disease pathology. Attempts to therapeutically deliver NO via organic nitrates (e.g. glyceryl trinitrate, GTN) to reduce blood pressure in hypertensives have been largely unsuccessful. However, in recent years inorganic (or ‘dietary’) nitrate has been identified as a potential solution for NO delivery through its sequential chemical reduction via the enterosalivary circuit. With dietary nitrate found in abundance in vegetables this review discusses epidemiological, pre-clinical and clinical data supporting the idea that dietary nitrate could represent a cheap and effective dietary intervention capable of reducing blood pressure and thereby improving cardiovascular health.

Inflammation has been shown to play an important role in the mechanisms involved in the pathogenesis of hypertension. Accordingly, innate and adaptive immune responses participate in blood pressure elevation. Here, we describe recent immunity studies focusing on novel inflammatory mechanisms during the hypertensive process. Different subpopulations of cells involved in innate and adaptive immune responses, such as monocyte/macrophages and dendritic cells on the one hand and B and T lymphocytes on the other hand, play roles leading to vascular injury in hypertension. Innate lymphoid cells, including natural killer cells and γ/δ T cells, have recently been demonstrated to participate in hypertensive mechanisms triggering vascular inflammation. In summary, we discuss the evidence of interaction of these different inflammatory and immune components in both experimental models and in humans during the development of hypertension.

Bisphenol A (BPA) exposure has become one of the most common environmental chemical exposures in humans. There is growing evidence regarding an association between BPA exposure, hypertension, and cardiovascular diseases (CVD). If BPA exposure is indeed associated with raised blood pressure and CVD, it would be a major public health problem. Therefore, we reviewed the epidemiological, laboratory, and clinical trial evidence for an association between BPA exposure, CVD, and hypertension, and discussed the possible mechanisms in this article. Cross-sectional studies in various ethnicities suggested a possible association between BPA exposure and hypertension; this association was supported by a panel study and a randomized clinical trial. Despite the discordance among cross-sectional studies about an association between BPA exposure and CVD, a longitudinal study shows that BPA exposure is a risk factor for CVD. The effects of BPA exposure such as endocrinal disturbance, induction of oxidative stress and inflammation, epigenetic change, and links with other chronic diseases may highlight a possible mechanism between BPA exposure, CVD, and hypertension. To clarify the causal relationship, well-designed studies are needed in the future.