scholarly journals Tempol Alters Urinary Extracellular Vesicle Lipid Content and Release While Reducing Blood Pressure during the Development of Salt-Sensitive Hypertension

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1804
Author(s):  
Kevin M. Chacko ◽  
Mohammad-Zaman Nouri ◽  
Whitney C. Schramm ◽  
Zeeshan Malik ◽  
Lauren P. Liu ◽  
...  

Salt-sensitive hypertension resulting from an increase in blood pressure after high dietary salt intake is associated with an increase in the production of reactive oxygen species (ROS). ROS are known to increase the activity of the epithelial sodium channel (ENaC), and therefore, they have an indirect effect on sodium retention and increasing blood pressure. Extracellular vesicles (EVs) carry various molecules including proteins, microRNAs, and lipids and play a role in intercellular communication and intracellular signaling in health and disease. We investigated changes in EV lipids, urinary electrolytes, osmolality, blood pressure, and expression of renal ENaC and its adaptor protein, MARCKS/MARCKS Like Protein 1 (MLP1) after administration of the antioxidant Tempol in salt-sensitive hypertensive 129Sv mice. Our results show Tempol infusion reduces systolic blood pressure and protein expression of the alpha subunit of ENaC and MARCKS in the kidney cortex of hypertensive 129Sv mice. Our lipidomic data show an enrichment of diacylglycerols and monoacylglycerols and reduction in ceramides, dihydroceramides, and triacylglycerols in urinary EVs from these mice after Tempol treatment. These data will provide insight into our understanding of mechanisms involving strategies aimed to inhibit ROS to alleviate salt-sensitive hypertension.

1999 ◽  
Vol 18 (6) ◽  
pp. 203-209 ◽  
Author(s):  
Olli Arjamaa ◽  
Lauri Turunen ◽  
Tero Malkinen ◽  
Jaana Laitinen ◽  
Juhani Leppaluoto ◽  
...  

JAMA ◽  
1983 ◽  
Vol 250 (3) ◽  
pp. 365 ◽  
Author(s):  
Robert A. Holden

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.R Choi

Abstract   Excessive dietary salt intake is associated with an increased risk of hypertension. Salt sensitivity, i.e., an elevation in blood pressure in response to high dietary salt intake, has been associated with a high risk of cardiovascular disease and mortality. We investigated whether a causal association exists between dietary sodium intake and hypertension risk using Mendelian randomization (MR). We performed an MR study using data from a large genome-wide association study comprising 15,034 Korean adults in a community-based cohort study. A total of 1,282 candidate single nucleotide polymorphisms associated with dietary sodium intake, such as rs2960306, rs4343, and rs1937671, were selected as instrumental variables. The inverse variance weighted method was used to assess the evidence for causality. Higher dietary sodium intake was associated with salt-sensitive hypertension risk. The variants of SLC8E1 rs2241543 and ADD1 rs16843589 were strongly associated with increased blood pressure. In the logistic regression model, after adjusting for age, gender, smoking, drinking, exercise, and body mass index, the GRK4 rs2960306TT genotype was inversely associated with hypertension risk (OR = 0.356, 95% CI = 0.236–0.476). However, the 2350GG genotype (ACE rs4343) exhibited a 2.11-fold increased hypertension risk (OR = 2.114, 95% CI = 2.004–2.224) relative to carriers of the 2350AA genotype, after adjusting for confounders. MR analysis revealed that the odds ratio for hypertension per 1 mg/day increment of dietary sodium intake was 2.24 in participants with the PRKG1 rs12414562 AA genotype. Our findings suggest that dietary sodium intake may be causally associated with hypertension risk. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education (2017R1D1A3B03034119, 2014M3C9A3064552), and the KRIBB Initiative program. This research was also supported by the Medical Research Center Program (2017R1A5A2015369). This work was supported (in part) by the Yonsei University Research Fund 2017. Bioresources for this study were provided by the National Biobank of Korea and the Centers for Disease Control and Prevention, Republic of Korea (2017-009).


Author(s):  
Mariyam Khwaja

Background: Healthy dietary practice is an important lifestyle modification and one of the key adjuncts to pharmacotherapy in management of hypertension. A modest reduction in salt intake of 5 gm/day lowered blood pressure by 7/4 mmHg diastolic in hypertensive patients. Despite knowledge about the ill consequences, many people continue to consume high levels of salt in their diet. To motivate people to reduce salt in their diet, a solid understanding of barriers encountered by those under salt reduction recommendation is necessary. Hence, this study was conducted with the aim of identifying the barriers to dietary salt reduction among hypertensive patients.Methods: A community based cross sectional study was conducted on a sample of 356 hypertensive patients in field practice areas (urban and rural) in Department of Community Medicine, JNMC, AMU, Aligarh. A pretested semi-structured questionnaire was used for the study. Compliance to dietary salt intake was assessed by calculating average salt intake per person per day. The tenets of health belief model were used to examine the key determinants of human behavior. Analysis was done by using correlation, proportions, chi-square and multiple linear regression.Results: 31.4% of the participants took salt <5 gm per day. A significant association was noticed with area, religion, social class, family size, perceived benefits and perceived susceptibility. A significant positive correlation was seen with total adherence score and family size.Conclusions: A lot of barriers hinder the compliance to dietary salt reduction. Health Education stressing the role of salt reduction in control of blood pressure is recommended.


JAMA ◽  
1983 ◽  
Vol 250 (3) ◽  
pp. 365-369 ◽  
Author(s):  
R. A. Holden

Sign in / Sign up

Export Citation Format

Share Document