Special Issue "Oxidative Stress and Salt-Sensitive Hypertension"
A special issue of Antioxidants (ISSN 2076-3921).
Deadline for manuscript submissions: closed (31 August 2017).
Prof. Dr. Dewan S. A. Majid
Salt sensitive hypertension (SSH) is characterized by increases in blood pressure in response to increases in dietary salt intake and is associated with an enhanced risk of cardiovascular and renal morbidity, particularly with the aging population. The increasing cost of the management of patients with SSH and associated renal injury (RI), which are hallmarks of chronic cardiovascular (CVD) and renal diseases (CKD), has been posing a major socio-economic burden on population health and national economies. The inability to control these CVD and CKD episodes and their complications in the human population are mainly due to our lack of comprehensive understanding of the pathophysiology of SSH. Although researchers have sought for decades to understand how salt sensitivity develops in humans, the mechanisms responsible for the increases in blood pressure in response to high salt (HS) intake are complex and only partially understood. Despite abundant epidemiological, experimental, and interventional observations, demonstrating an association between salt and blood pressure, skepticism still remains as to how HS intake can be mechanistically linked to increase in blood pressure. Inability to explain why salt raises blood pressure in some individuals (described as “salt sensitive”) but not in others (termed as “salt resistant”) has hampered the development of a comprehensive theory as to what causes high blood pressure in most cases. Inappropriate renal responses to HS intake during oxidative stress condition modulate renal hemodynamics and tubular reabsorptive function to enhance sodium retention that leads to the development of SSH. In this review series, “Oxidative Stress and Salt-Sensitive Hypertension” will include invited mini-reviews covering exciting areas related to dysregulation of renal function by reactive oxygen species, such as nitric oxide (NO), superoxide (O2−) in the pathophysiology of SSH and RI. In future studies, emphasis should be given to understand how NO exerts its protective role against the action of O2− since the chemical reaction between these two molecules usually results in the formation of another oxidant radical, peroxynitrite (ONOO−). A review article on the implications of ONOO− formation in the pathophysiology of SSH would be helpful in future efforts to delineate the complex biological actions of these radical compounds in the kidney. It is known that an enhancement in angiotensinogen (AGT) generation in the kidney is associated with progression of SSH and RI. This renal generation of AGT increased paradoxically during HS intake in elevated angiotensin II (AngII) condition inducing oxidative stress but not in normal condition. A general consensus that also persists is that, SSH and RI are inflammatory conditions induced by various pro-inflammatory cytokines, particularly tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which are released in the condition of oxidative stress induced by NO deficiency or elevated AngII level. There is also an emerging issue that a differential activation of TNF receptor type 1 and type 2 signaling pathways may be involved in enhanced intrarenal AGT formation during HS intake in the conditions of elevated AngII or NO deficiency. Recent studies also show that gender differences also influence the overall regulation of oxidative balance. A review article will also be included to dissect the link between sex hormones and the oxidative stress mechanisms that differentiate the patho-physiological processes of SSH between male and female. Overall, we hope that these mini-reviews included in this section would enhance the enthusiasm among the researchers to delineate the complexities of the interaction between oxidative stress, renin-angiotensin system and inflammatory cytokines, which would further unravel the mechanistic mysteries influencing the salt sensitivity and hypertension in humans and will help to identify the reason for the heterogeneity in the blood pressure response to HS intake in the general population.
Prof. Dr. Dewan S. A. Majid
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- Salt sensitivity
- Oxidative stress
- Nitric oxide
- Angiotensin II
- Inflammatory cytokines
- Tumor necrosis factor-alpha