Proposition of a Feasible Protocol to Evaluate Salt Sensitivity in a Population-Based Setting.

Kato, Norihiro; Kanda, Tomo; Sagara, Miki; Bós, Ângelo José Gonçalves; Moriguchi, Emílio Hideyuki; Moriguchi, Yukio; Yamori, Yukio

doi:10.1291/hypres.25.801

Cited by 10 publications

(12 citation statements)

References 21 publications

(20 reference statements)

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“…Efforts to use simpler and shorter protocols 375 have failed validation. 376 Four subsequent studies 4,385,387,388 were performed to assess the congruence of BP responses to the rapid intravenous saline loading plus diuretic-induced sodium and volume depletion protocol with slower dietary sodium intake approaches. These comparisons were consistently significant.…”

Section: Reproducibility Of the Bp Response To Sodiummentioning

confidence: 99%

Salt Sensitivity of Blood Pressure

Elijovich¹,

Weinberger²,

Anderson³

et al. 2016

Hypertension

370

230

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The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on January 23, 2016, and the American Heart Association Executive Committee on February 23, 2016. A copy of the document is available at http://professional.heart.org/statements by using either "Search for Guidelines & Statements" or the "Browse by Topic" area. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@ wolterskluwer.com.The American Heart Association requests that this document be cited as follows: Elijovich F, Weinberger MH, Anderson CAM, Appel LJ, Bursztyn M, Cook NR, Dart RA, Newton-Cheh CH, Sacks FM, Laffer CL; on behalf of the American Heart Association Professional and Public Education Committee of the Council on Hypertension; Council on Functional Genomics and Translational Biology; and Stroke Council. Salt sensitivity of blood pressure: a scientific statement from the American Heart Association. Hypertension. 2016;68:e7-e46. doi: 10.1161/HYP.0000000000000047.Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://professional.heart.org/statements. Select the "Guidelines & Statements" drop-down menu, then click "Publication Development."Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/CopyrightPermission-Guidelines_UCM_300404_Article.jsp. A link to the "Copyright Permissions Request Form" appears on the right side of the page. Figure 2 shows the major effect of aging in increasing the prevalence of SSBP in both normotensive and hypertensive subjects. An important and encouraging observation is that the multiple phenotypic characteristics described in pure SS strains of rodents reproduce those observed in humans, indicating that the phenotypic cluster of SSBP can be brought out in humans by the current techniques used in carefully controlled research. Additionally, despite the unquestionable influence of environmental factors in the determination of SSBP in humans, estimates of its heritability have been as high as 74% in blacks 9 and 50% in Chinese subjects, 10 both higher than those for hypertension. Salt Sensitivity of Blood PressureAn important issue is the clinical significance of the SSBP phenotype. There was increasing understanding that it represents an abnormality. The reasons w...

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Section: Reproducibility Of the Bp Response To Sodiummentioning

confidence: 99%

Salt Sensitivity of Blood Pressure

Elijovich¹,

Weinberger²,

Anderson³

et al. 2016

Hypertension

370

230

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show abstract

“…The incidence of SS, defined as MAP >10% on day 6 of the high Na + protocol relative to day 6 of the low Na + protocol, was 48%. The most convenient method to determine SS is by the intravenous Na + loading and furosemide method [13,50], but its accuracy of has been questioned [14–16] and thus the advocating of a 14 day test (7 days of low Na + and 7 days of high Na + intake) [14–16,51]. To overcome these dietary protocol limitations, we developed a robust and convenient SS diagnostic test, using urine specimens from subjects whose salt-sensitive, SR, and ISS phenotypes were based on the generally accepted 14-day oral salt loading protocol [14–16,51,52].…”

Section: Discussionmentioning

confidence: 99%

“…Despite its high prevalence and significant morbidity and mortality, the diagnosis of SS can only be determined using an extensive dietary salt loading and salt depletion study performed in an inpatient setting (i.e., clinical research center). Furthermore, the results obtained with a simpler and more rapid protocol [13] correlate poorly with the more generally accepted 2-week controlled Na + diet protocol [14–17]. …”

Section: Introductionmentioning

confidence: 99%

A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: The virtual renal biopsy

Gildea

Lahiff

Sciver

et al. 2013

Clinica Chimica Acta

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Background Salt sensitivity (SS) of blood pressure (BP) affects 25% of adults, shares comorbidity with hypertension, and has no convenient diagnostic test. We tested the hypothesis that urine-derived exfoliated renal proximal tubule cells (RPTCs) could diagnose the degree of an individual's SS of BP. Methods Subjects were selected who had their SS of BP determined 5 y prior to this study (salt-sensitive: ≥7 mm Hg increase in mean arterial pressure (MAP) following transition from a random weekly diet of low (10 mmol/day) to high (300 mmol/day) sodium (Na+) intake, N = 4; inverse salt-sensitive (ISS): ≥7 mm Hg increase in MAP transitioning from a high to low Na+ diet, N = 3, and salt-resistant (SR): <7 mm Hg change in MAP transitioned on either diet, N = 5). RPTC responses to 2 independent Na+ transport pathways were measured. Results There was a negative correlation between the degree of SS and dopamine-1 receptor (D1R) plasma membrane recruitment (y = −0.0107x + 0.68 relative fluorescent units (RFU), R2 = 0.88, N = 12, P < 0.0001) and angiotensin II-stimulated intracellular Ca++ (y = −0.0016x + 0.0336, R2 = 0.7112, P < 0.001, N = 10) concentration over baseline. Conclusions Isolating RPTCs from urine provides a personalized cell-based diagnostic test of SS index that offers advantages over a 2-week controlled diet with respect to cost and patient compliance. Furthermore, the linear relationship between the change in MAP and response to 2 Na+ regulatory pathways suggests that an individual's RPTC response to intracellular Na+ is personalized and predictive.

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“…Apparently, the most reliable method requires putting patients on a diet with normal sodium intake for 5 to 7 days, followed by a reduction of sodium intake for 5 to 7 days, and then high sodium dietary intake for 5 to 7 days [7, 8]. Although a shorter 2-week protocol has been suggested, there is only a 0.69 correlation coefficient between blood pressures obtained in shorter protocols [9] and the definitive method of strict dietary regimen [5–8]. The increase in blood pressure in response to an increase in sodium in the diet depends on the amount of sodium intake [10], sodium as halide salts [11], and ethnicity [11].…”

Section: Introductionmentioning

confidence: 99%

Genetics of Salt-Sensitive Hypertension

Sanada¹,

2010

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The assessment of salt sensitivity of blood pressure is difficult because of the lack of universal consensus on definition. Regardless of the variability in the definition of salt sensitivity, increased salt intake, independent of the actual level of blood pressure, is also a risk factor for cardiovascular morbidity and mortality and kidney disease. A modest reduction in salt intake results in an immediate decrease in blood pressure, with long-term beneficial consequences. However, some have suggested that dietary sodium restriction may not be beneficial to everyone. Thus, there is a need to distinguish salt-sensitive from salt-resistant individuals, but it has been difficult to do so with phenotypic studies. Therefore, there is a need to determine the genes that are involved in salt sensitivity. This review focuses on genes associated with salt sensitivity, with emphasis on the variants associated with salt sensitivity in humans that are not due to monogenic causes. Special emphasis is given to gene variants associated with salt sensitivity whose protein products interfere with cell function and increase blood pressure in transgenic mice.

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Proposition of a Feasible Protocol to Evaluate Salt Sensitivity in a Population-Based Setting.

Cited by 10 publications

References 21 publications

Salt Sensitivity of Blood Pressure

Salt Sensitivity of Blood Pressure

A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: The virtual renal biopsy

Genetics of Salt-Sensitive Hypertension

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