Special Issue "Oxidative Stress and Salt-Sensitive Hypertension"

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 August 2017).

Special Issue Editor

Guest Editor
Prof. Dr. Dewan S. A. Majid

Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, LA, USA
Website | E-Mail
Interests: inflammatory cytokines, tumor necrosis factor-alpha (TNF-α), salt-sensitive hypertension (SSH), renal injury (RI), AngII, NO

Special Issue Information

Dear Colleagues,

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
Guest Editor

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Keywords

  • Salt sensitivity
  • Hypertension
  • Oxidative stress
  • Nitric oxide
  • Superoxide
  • Peroxynitrite
  • Angiotensinogen
  • Angiotensin II
  • Inflammatory cytokines
  • Tumor necrosis factor-alpha

Published Papers (3 papers)

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Review

Open AccessReview
Transcription Factor ETS-1 and Reactive Oxygen Species: Role in Vascular and Renal Injury
Antioxidants 2018, 7(7), 84; https://doi.org/10.3390/antiox7070084
Received: 23 April 2018 / Revised: 15 June 2018 / Accepted: 2 July 2018 / Published: 3 July 2018
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Abstract
The E26 avian erythroblastosis virus transcription factor-1 (ETS-1) is a member of the ETS family and regulates the expression of a variety of genes including growth factors, chemokines and adhesion molecules. Although ETS-1 was discovered as an oncogene, several lines of research show [...] Read more.
The E26 avian erythroblastosis virus transcription factor-1 (ETS-1) is a member of the ETS family and regulates the expression of a variety of genes including growth factors, chemokines and adhesion molecules. Although ETS-1 was discovered as an oncogene, several lines of research show that it is up-regulated by angiotensin II (Ang II) both in the vasculature and the glomerulus. While reactive oxygen species (ROS) are required for Ang II-induced ETS-1 expression, ETS-1 also regulates the expression of p47phox, which is one of the subunits of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and a major source of ROS in the kidney and vasculature. Thus, there appears to be a positive feedback between ETS-1 and ROS. ETS-1 is also upregulated in the kidneys of rats with salt-sensitive hypertension and plays a major role in the development of end-organ injury in this animal model. Activation of the renin angiotensin system is required for the increased ETS-1 expression in these rats, and blockade of ETS-1 or haplodeficiency reduces the severity of kidney injury in these rats. In summary, ETS-1 plays a major role in the development of vascular and renal injury and is a potential target for the development of novel therapeutic strategies to ameliorate end-organ injury in hypertension. Full article
(This article belongs to the Special Issue Oxidative Stress and Salt-Sensitive Hypertension)
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Open AccessReview
Effects of Reactive Oxygen Species on Tubular Transport along the Nephron
Antioxidants 2017, 6(2), 23; https://doi.org/10.3390/antiox6020023
Received: 31 January 2017 / Revised: 15 March 2017 / Accepted: 18 March 2017 / Published: 23 March 2017
Cited by 6 | PDF Full-text (703 KB) | HTML Full-text | XML Full-text
Abstract
Reactive oxygen species (ROS) are oxygen-containing molecules naturally occurring in both inorganic and biological chemical systems. Due to their high reactivity and potentially damaging effects to biomolecules, cells express a battery of enzymes to rapidly metabolize them to innocuous intermediaries. Initially, ROS were [...] Read more.
Reactive oxygen species (ROS) are oxygen-containing molecules naturally occurring in both inorganic and biological chemical systems. Due to their high reactivity and potentially damaging effects to biomolecules, cells express a battery of enzymes to rapidly metabolize them to innocuous intermediaries. Initially, ROS were considered by biologists as dangerous byproducts of respiration capable of causing oxidative stress, a condition in which overproduction of ROS leads to a reduction in protective molecules and enzymes and consequent damage to lipids, proteins, and DNA. In fact, ROS are used by immune systems to kill virus and bacteria, causing inflammation and local tissue damage. Today, we know that the functions of ROS are not so limited, and that they also act as signaling molecules mediating processes as diverse as gene expression, mechanosensation, and epithelial transport. In the kidney, ROS such as nitric oxide (NO), superoxide (O2), and their derivative molecules hydrogen peroxide (H2O2) and peroxynitrite (ONO2) regulate solute and water reabsorption, which is vital to maintain electrolyte homeostasis and extracellular fluid volume. This article reviews the effects of NO, O2, ONO2, and H2O2 on water and electrolyte reabsorption in proximal tubules, thick ascending limbs, and collecting ducts, and the effects of NO and O2 in the macula densa on tubuloglomerular feedback. Full article
(This article belongs to the Special Issue Oxidative Stress and Salt-Sensitive Hypertension)
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Figure 1

Open AccessReview
Na/K-ATPase Signaling and Salt Sensitivity: The Role of Oxidative Stress
Antioxidants 2017, 6(1), 18; https://doi.org/10.3390/antiox6010018
Received: 23 January 2017 / Revised: 10 February 2017 / Accepted: 22 February 2017 / Published: 2 March 2017
Cited by 4 | PDF Full-text (437 KB) | HTML Full-text | XML Full-text
Abstract
Other than genetic regulation of salt sensitivity of blood pressure, many factors have been shown to regulate renal sodium handling which contributes to long-term blood pressure regulation and have been extensively reviewed. Here we present our progress on the Na/K-ATPase signaling mediated sodium [...] Read more.
Other than genetic regulation of salt sensitivity of blood pressure, many factors have been shown to regulate renal sodium handling which contributes to long-term blood pressure regulation and have been extensively reviewed. Here we present our progress on the Na/K-ATPase signaling mediated sodium reabsorption in renal proximal tubules, from cardiotonic steroids-mediated to reactive oxygen species (ROS)-mediated Na/K-ATPase signaling that contributes to experimental salt sensitivity. Full article
(This article belongs to the Special Issue Oxidative Stress and Salt-Sensitive Hypertension)
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