Relationships Between Salt Sensitivity of Blood Pressure and Sympathetic Nervous System Activity: A Short Review of Evidence

Strazzullo, Pasquale; Barbato, Antonio; Vuotto, P; Galletti, Ferruccio

doi:10.1081/ceh-100001194

Cited by 41 publications

(32 citation statements)

References 21 publications

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“…These observations were consistent with many others in which subjects with the metabolic syndrome, who are insulin resistant and SS, have increased sympathetic nervous system activity and heart rates. 39,[425][426][427] Another characteristic of many groups of hypertensive patients (eg, secondary hypertension, obstructive sleep apnea, chronic renal insufficiency) is a diminished sleep-associated reduction in BP (nondipping of BP), which is known to have detrimental prognostic implications. Subjects with features of the SS hypertensive phenotype such as the metabolic syndrome also have a high prevalence of nondipping.…”

Section: Surrogate Markers Of Ssbp In Humansmentioning

confidence: 99%

Salt Sensitivity of Blood Pressure

Elijovich¹,

Weinberger²,

Anderson³

et al. 2016

Hypertension

359

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: Surrogate Markers Of Ssbp In Humansmentioning

confidence: 99%

Salt Sensitivity of Blood Pressure

Elijovich¹,

Weinberger²,

Anderson³

et al. 2016

Hypertension

359

230

View full text Add to dashboard Cite

show abstract

“…However, the mechanisms involved in this alteration are not fully elucidated. Vasoconstriction of renal arteries due to activation or inadequate suppression of neuroendocrine systems such as the renin-angiotensin system [24,25] and the sympathetic nervous system [26] may be involved in this process. A deficiency of vasodilator substances such as dopamine [27], kallikrein [28], or nitric oxide (NO) [29] may also contribute to this alteration.…”

Section: Discussionmentioning

confidence: 99%

Effect of sodium overload on renal function of offspring from diabetic mothers

et al. 2008

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The aim if this study was to evaluate the effect of sodium overload on blood pressure and renal function in the offspring of diabetic rat mothers. Diabetes was induced with a single dose of streptozotocin before mating. Experimental groups were control (C), offspring from diabetic mother (D), control with sodium chloride (NaCl) overload (CS), and offspring from diabetic mother submitted to NaCl overload (DS). After weaning, all groups received food ad libitum; groups C and D had water ad libitum, and CS and DS received NaCl 0.15 M as drinking water. Renal morphology and function were evaluated in 3-month-old rats. Glomerular area, macrophage infiltration, interlobular artery wall thickness, and renal vascular resistance were significantly increased in CS, D, and DS compared with C. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were decreased in CS and D compared with C. In DS, GFR and fractional filtration were increased, suggesting a state of hyperfiltration. Hypertension was observed in groups D, CS, and DS from 2 months on and was more severe in DS. Our data suggest that diabetes during intrauterine development and salt overload beginning at an early age can cause hypertension and renal injury. When these conditions were associated, morphological and functional changes were much more intense, suggesting acceleration in the process of kidney injury.

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“…They may include vasoconstriction of glomerular arterioles attributable to activation (or inadequate suppression) of neuroendocrine systems 6 such as the renin-angiotensin system 23,24 or the sympathetic nervous system. 25 Possibly, these elements play an important role in returning renal blood flow to control levels in IUS animals. Although high sodium intake, via an increased response of renal nerves and the renin-angiotensin system locally, restores renal hemodynamic function to control levels, systemically, it might be responsible for the increased blood pressure in IUS animals.…”

Section: Discussionmentioning

confidence: 99%

High Sodium Intake Increases Blood Pressure and Alters Renal Function in Intrauterine Growth–Retarded Rats

et al. 2005

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Abstract-A suboptimal fetal environment increases the risk to develop cardiovascular disease in the adult. We reported previously that intrauterine stress in response to reduced uteroplacental blood flow in the pregnant rat limits fetal growth and compromises renal development, leading to an altered renal function in the adult offspring. Here we tested the hypothesis that high dietary sodium intake in rats with impaired renal development attributable to intrauterine stress, results in increased blood pressure, altered renal function, and organ damage. In rats, intrauterine stress was induced by bilateral ligation of the uterine arteries at day 17 of pregnancy. At the age of 12 weeks, the offspring was given high-sodium drinking water (2% sodium chloride). At the age of 16 weeks, rats were instrumented for monitoring of blood pressure and renal function. After intrauterine stress, litter size and birth weight were reduced, whereas hematocrit at birth was increased. Renal blood flow, glomerular filtration rate, and the glomerular filtration fraction were increased significantly after intrauterine stress. High sodium intake did not change renal function and blood pressure in control animals. However, during high sodium intake in intrauterine stress offspring, renal blood flow, glomerular filtration rate, and the filtration fraction were decreased, and blood pressure was increased. In addition, these animals developed severe albuminuria, an important sign of renal dysfunction. Thus, a suboptimal fetal microenvironment, which impairs renal development, results in sodium-dependent hypertension and albuminuria. Key Words: hypertension, sodium-dependent Ⅲ sodium A healthy intrauterine environment is prerequisite for normal development. A suboptimal intrauterine environment may permanently alter some tissues and organs that enable the fetus to survive in utero but cause a predisposition to (cardiovascular) disease later in life. 1 Particularly, the development of the kidney can be affected by this process of fetal programming. 2 A possible mechanism might be an impaired nephrogenesis as a result of a suboptimal intrauterine environment. This may lead to reduced nephron endowment during development, which is associated with high blood pressure 3 and renal dysfunction 4 in the adult. Previous studies in our laboratory have shown that a suboptimal intrauterine environment, induced by bilateral ligation of the uterine arteries of pregnant rats, resulted in a decreased glomerular number, an increased glomerular size, and an altered renal function in the adult offspring. In young adults, we could not demonstrate a change in blood pressure as a result of a suboptimal fetal environment, but we have shown that the renal compensatory capacity after unilateral nephrectomy is reduced. 5 Not only fetal programming, but also dietary influences such as high sodium intake, increase the risk of cardiovascular and renal diseases, independently of other cardiovascular risk factors, including blood pressure. 6 High sodium intake may have de...

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Relationships Between Salt Sensitivity of Blood Pressure and Sympathetic Nervous System Activity: A Short Review of Evidence

Cited by 41 publications

References 21 publications

Salt Sensitivity of Blood Pressure

Salt Sensitivity of Blood Pressure

Effect of sodium overload on renal function of offspring from diabetic mothers

High Sodium Intake Increases Blood Pressure and Alters Renal Function in Intrauterine Growth–Retarded Rats

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