Current Hypertension Reviews最新文献

Increased applications of pesticides, mainly in agriculture and public health, have resulted in increased chances of human exposure to pesticides. Chronic exposure to pesticides has been implicated in several human diseases, including cardiovascular diseases. Cardiovascular diseases are broadly used for various heart pathological conditions, including a defect in blood vessels, and they include myocardial infarction, atherosclerosis, stroke, cardiomyopathy, coronary heart disease, etc. In this review, the association between human exposure to pesticides and the development of cardiovascular diseases was discussed using epidemiological and laboratory data. The toxicokinetics of pesticides in humans was reviewed, as well as the risk factors for cardiovascular diseases. The important role of oxidative stress principally the induction of reactive oxygen species as the signaling molecules for various signaling pathways involved in pesticides-induced cardiovascular disease, was discussed.

Most of the systemic blood vessels are surrounded by the perivascular adipose tissue (PVAT). Healthy PVAT is anticontractile and anti-inflammatory, but a dysfunctional PVAT has been suggested to link cardiometabolic risk factors to vascular dysfunction. Vascular oxidative stress is an important pathophysiological event in cardiometabolic complications of obesity, type 2 diabetes, and hypertension. PVAT-derived adipocytes generate reactive oxygen species (ROS) including superoxide anion and hydrogen peroxide that might signal to the vascular wall. Therefore, an abnormal generation of ROS by PVAT emerges as a potential pathophysiological mechanism underlying vascular injury. This review summarizes new findings describing ROS production in the PVAT of several vascular beds, major sources of ROS in this tissue including mitochondria, NADPH oxidase and eNOS uncoupled, and finally, changes in ROS production affecting vascular function in the presence of cardiometabolic risk factors and diseases.

Management of arterial hypertension in patients with chronic kidney disease (CKD) remains a major challenge due to its high prevalence and associations with cardiovascular disease (CVD) and CKD progression. Several clinical trials and meta-analyses have demonstrated that aggressive treatment of hypertension in patients with and without CKD lowers the risk of CVD and all-cause mortality, nevertheless the effects of blood pressure (BP) lowering in terms of renal protection or harm remain controversial. Both home and ambulatory BP estimation have shown that patients with CKD display abnormal BP patterns outside of the office and further investigation is required, so as to compare the association of ambulatory versus office BP measurements with hard outcomes and adjust treatment strategies accordingly. Although renin-angiotensin system blockade appears to be beneficial in patients with advanced CKD, especially in the setting of proteinuria, discontinuation of renin-angiotensin system inhibition should be considered in the setting of frequent episodes of acute kidney injury or hypotension while awaiting the results of ongoing trials. In light of the new evidence in favor of renal denervation in arterial hypertension, the indications and benefits of its application in individuals with CKD need to be clarified by future studies. Moreover, the clinical utility of the novel players in the pathophysiology of arterial hypertension and CKD, such as microRNAs and the gut microbiota, either as markers of disease or as therapeutic targets, remains a subject of intensive research.

Background: Disruption of redox signaling is a common pathophysiological mechanism observed in several diseases. In hypertension, oxidative stress, resulted either from enhances in Reactive Oxygen Species (ROS) production or decreases in antioxidant defenses, is associated with increase in blood pressure, endothelial dysfunction and vascular remodeling. Although the role of oxidative stress in the development of hypertension is well known, it is still unclear if this process is a cause or a consequence of tissue changes in hypertension. Indeed, unbalanced ROS formation results in several detrimental effects that contribute to hypertension, including reduction in nitric oxide bioavailability and activation of metalloproteinases. Additionally, ROS may also directly react with lipids, proteins and DNA, thereby contributing to tissue damage associated with hypertension. Therefore, a deep understanding of the role of oxidative stress in hypertension is essential to comprehend its pathophysiology and to identify new therapeutic targets.

Conclusion: This mini-review discusses the main enzymatic sources of oxidants and the major antioxidant defenses in the vasculature, followed by the effects of oxidative stress in hypertension, highlighting endothelial dysfunction, vascular remodeling and tissue damage.