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Biomedicines
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State-of-the-Art Hypertension and Biomedicine in the USA
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State-of-the-Art Hypertension and Biomedicine in the USA

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 6558

Special Issue Editors

Dr. Pedro A. José

E-Mail Website
Guest Editor
Medicine and Physiology/Pharmacology, School of Medicine and Health Sciences, The George Washington University, Washington, DC, USA
Interests: hypertension; renal physiology; ion transport; oxidative stress; pharmacogenomics
Special Issues, Collections and Topics in MDPI journals
Dr. Robin A. Felder

E-Mail Website
Guest Editor
Department of Pathology, University of Virginia, Charlottesville, VA 22903, USA
Interests: hypertension; renal physiology; ion transport; oxidative stress; pharmacogenomics

Special Issue Information

Dear Colleagues,

The long-term regulation of blood pressure rests on renal and non-renal mechanisms. The gastrointestinal tract has to be integrated in the overall regulation of sodium balance and blood pressure because it is the first organ exposed to ingested sodium. The gut microbiota can regulate about 10% of the host’s transcriptome, especially those genes related to immunity, cell proliferation, and metabolism. Hypertension develops with chronically increased sodium intake when sodium that accumulates in the body can no longer be sequestered (e.g., skin), extracellular fluid volume is expanded, and compensatory neural, hormonal, and pressure-natriuresis mechanisms fail. However, sodium is not the only mineral that can affect blood pressure. Moreover, sodium can affect overall health independent of blood pressure regulation. Thus, it is important to test the effect of minerals on blood pressure regulation-related and unrelated mechanisms, such as studying renal tubule cells shed in the urine. The changing environment has to be put into consideration into all the above mechanisms in the pathogenesis of hypertension.

We invite authors to contribute to this Special Issue of biomedicine and blood pressure on topics related to:

  1. Organ-to-organ communication in the regulation of blood pressure, e.g., brain and kidney, gut and kidney, gut, brain, and kidney;
  2. Microbiota and blood pressure regulation;
  3. Tissue sodium storage and hypertension: role of non-traditional organs in the pathogenesis of hypertension (skin and blood pressure);
  4. Sodium and other minerals in the regulation of blood pressure and blood pressure-dependent and -independent disease;
  5. Environment and blood pressure regulation;
  6. Non-invasive tests to determine nephron-segment specific tests of renal function (urine).

Dr. Robin A. Felder
Dr. Pedro A. José
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • organ crosstalk
  • microbiome
  • tissue sodium storage
  • minerals and blood pressure
  • environment and blood pressure
  • urine biomarkers

Published Papers (3 papers)

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15 pages, 2960 KiB  
Article
Intrarenal Dopaminergic System Is Dysregulated in SS-Resp18mutant Rats
by Usman M. Ashraf, Ealla Atari, Fawaz Alasmari, Harshal Waghulde, Vikash Kumar, Youssef Sari, Sonia M. Najjar, Pedro A. Jose and Sivarajan Kumarasamy
Biomedicines 2023, 11(1), 111; https://doi.org/10.3390/biomedicines11010111 - 01 Jan 2023
Cited by 1 | Viewed by 1554
Abstract
The genetic and molecular basis of developing high blood pressure and renal disease are not well known. Resp18mutant Dahl salt-sensitive (SS-Resp18mutant) rats fed a 2% NaCl diet for six weeks have high blood pressure, increased renal fibrosis, and decreased [...] Read more.
The genetic and molecular basis of developing high blood pressure and renal disease are not well known. Resp18mutant Dahl salt-sensitive (SS-Resp18mutant) rats fed a 2% NaCl diet for six weeks have high blood pressure, increased renal fibrosis, and decreased mean survival time. Impairment of the dopaminergic system also leads to hypertension that involves renal and non-renal mechanisms. Deletion of any of the five dopamine receptors may lead to salt-sensitive hypertension. Therefore, we investigated the interaction between Resp18 and renal dopamine in SS-Resp18mutant and Dahl salt-sensitive (SS) rats. We found that SS-Resp18mutant rats had vascular dysfunction, as evidenced by a decrease in vasorelaxation in response to sodium nitroprusside. The pressure–natriuresis curve in SS-Resp18mutant rats was shifted down and to the right of SS rats. SS-Resp18mutant rats had decreased glomerular filtration rate and dopamine receptor subtypes, D1R and D5R. Renal dopamine levels were decreased, but urinary dopamine levels were increased, which may be the consequence of increased renal dopamine production, followed by secretion into the tubular lumen. The increased renal dopamine production in SS-Resp18mutant rats in vivo was substantiated by the increased dopamine production in renal proximal tubule cells treated with L-DOPA. Overall, our study provides evidence that targeted disruption of the Resp18 locus in the SS rat dysregulates the renal dopaminergic system. Full article
(This article belongs to the Special Issue State-of-the-Art Hypertension and Biomedicine in the USA)
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22 pages, 2705 KiB  
Article
Inverse Salt Sensitivity of Blood Pressure Is Associated with an Increased Renin-Angiotensin System Activity
by John J. Gildea, Peng Xu, Katie A. Schiermeyer, Wei Yue, Robert M. Carey, Pedro A. Jose and Robin A. Felder
Biomedicines 2022, 10(11), 2811; https://doi.org/10.3390/biomedicines10112811 - 04 Nov 2022
Cited by 2 | Viewed by 1938
Abstract
High and low sodium diets are associated with increased blood pressure and cardiovascular morbidity and mortality. The paradoxical response of elevated BP in low salt diets, aka inverse salt sensitivity (ISS), is an understudied vulnerable 11% of the adult population with yet undiscovered [...] Read more.
High and low sodium diets are associated with increased blood pressure and cardiovascular morbidity and mortality. The paradoxical response of elevated BP in low salt diets, aka inverse salt sensitivity (ISS), is an understudied vulnerable 11% of the adult population with yet undiscovered etiology. A linear relationship between the number of single nucleotide polymorphisms (SNPs) in the dopamine D2 receptor (DRD2, rs6276 and 6277), and the sodium myo-inositol cotransporter 2 (SLC5A11, rs11074656), as well as decreased expression of these two genes in urine-derived renal proximal tubule cells (uRPTCs) isolated from clinical study participants suggest involvement of these cells in ISS. Insight into this newly discovered paradoxical response to sodium is found by incubating cells in low sodium (LS) conditions that unveil cell physiologic differences that are then reversed by mir-485-5p miRNA blocker transfection and bypassing the genetic defect by DRD2 re-expression. The renin-angiotensin system (RAS) is an important counter-regulatory mechanism to prevent hyponatremia under LS conditions. Oversensitive RAS under LS conditions could partially explain the increased mortality in ISS. Angiotensin-II (AngII, 10 nmol/L) increased sodium transport in uRPTCs to a greater extent in individuals with ISS than SR. Downstream signaling of AngII is verified by identifying lowered expression of nuclear factor erythroid 2-related factor 2 (NRF2), CCCTC-binding factor (CTCF), and manganese-dependent mitochondrial superoxide dismutase (SOD2) only in ISS-derived uRPTCs and not SR-derived uRPTCs when incubated in LS conditions. We conclude that DRD2 and SLC5A11 variants in ISS may cause an increased low sodium sensitivity to AngII and renal sodium reabsorption which can contribute to inverse salt-sensitive hypertension. Full article
(This article belongs to the Special Issue State-of-the-Art Hypertension and Biomedicine in the USA)
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17 pages, 3717 KiB  
Article
Epithelial Sodium Channel Alpha Subunit (αENaC) Is Associated with Inverse Salt Sensitivity of Blood Pressure
by Peng Xu, Anastasia V. Sudarikova, Daria V. Ilatovskaya, John J. Gildea, Mahabuba Akhter, Robert M. Carey, Wei Yue, Pedro A. Jose and Robin A. Felder
Biomedicines 2022, 10(5), 981; https://doi.org/10.3390/biomedicines10050981 - 23 Apr 2022
Cited by 4 | Viewed by 2204
Abstract
Salt sensitivity of blood pressure (BP) refers to an increase in BP following an increase in dietary salt, which is associated with increased incidence of cardiovascular disease and early death. However, decreased sodium intake also increases mortality and morbidity. Inverse salt sensitivity (ISS), [...] Read more.
Salt sensitivity of blood pressure (BP) refers to an increase in BP following an increase in dietary salt, which is associated with increased incidence of cardiovascular disease and early death. However, decreased sodium intake also increases mortality and morbidity. Inverse salt sensitivity (ISS), defined as a paradoxical increase in BP on a low-salt diet, about 11% of the population, may be the cause of this phenomenon. The epithelial sodium channel (ENaC) is a major regulator of sodium reabsorption in the kidney. In this study, human renal tubular epithelial cells (hRTC) were cultured from the urine of phenotyped salt study participants. αENaC expression was significantly lower in ISS than salt resistant (SR) hRTC, while ENaC-like channel activity was dramatically increased by trypsin treatment in ISS cells analyzed by patch clamp. αENaC expression was also decreased under high-salt treatment and increased by aldosterone treatment in ISS cells. Moreover, the αENaC variant, rs4764586, was more prevalent in ISS. In summary, αENaC may be associated with ISS hypertension on low salt. These findings may contribute to understanding the mechanisms of ISS and low salt effect on morbidity and mortality. Full article
(This article belongs to the Special Issue State-of-the-Art Hypertension and Biomedicine in the USA)
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