Mechanisms and consequences of salt sensitivity and dietary salt intake

Basit Öğe Kaydı
dc.contributor.authorKanbay, Mehmet
dc.contributor.authorChen, Yabing
dc.contributor.authorSolak, Yalcin
dc.contributor.authorSanders, Paul W.
dc.date.accessioned2020-03-26T18:15:14Z
dc.date.available2020-03-26T18:15:14Z
dc.date.issued2011
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractPurpose of review Investigation into the underlying mechanisms of salt sensitivity has made important advances in recent years. This review examines in particular the effects of sodium and potassium on vascular function. Recent findings Sodium chloride (salt) intake promotes cutaneous lymphangiogenesis mediated through tissue macrophages and directly alters endothelial cell function, promoting increased production of transforming growth factor-beta (TGF-beta) and nitric oxide. In the setting of endothelial dysfunction, such as occurs with aging, diminished nitric oxide production exacerbates the vascular effects of TGF-beta, promoting decreased arterial compliance and hypertension. Dietary potassium intake may serve as an important countervailing influence on the effects of salt in the vasculature. Summary There is growing appreciation that, independently of alterations in blood pressure, dietary intake of sodium and potassium promotes functional changes in the vasculature and lymphatic system. These changes may protect against development of salt-sensitive hypertension. While salt sensitivity cannot be ascribed exclusively to these factors, perturbation of these processes promotes hypertension during high-salt intake. These studies add to the list of genetic and environmental factors that are associated with salt sensitivity, but in particular provide insight into adaptive mechanisms during high salt intake.en_US
dc.description.sponsorshipNational Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [R01 DK046199, R01 HL092215, P30 DK079337]; Office of Research and Development, Medical Research Service, Department of Veterans AffairsUS Department of Veteran Affairsen_US
dc.description.sponsorshipNational Institutes of Health grants, R01 DK046199 (PWS) and R01 HL092215 (YC), National Institutes of Health P30 DK079337 (George M. O'Brien Kidney and Urological Research Centers Program) (PWS) and the Office of Research and Development, Medical Research Service, Department of Veterans Affairs (YC and PWS) support this research.en_US
dc.identifier.doi10.1097/MNH.0b013e32834122f1en_US
dc.identifier.endpage43en_US
dc.identifier.issn1062-4821en_US
dc.identifier.issn1473-6543en_US
dc.identifier.issue1en_US
dc.identifier.pmid21088577en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage37en_US
dc.identifier.urihttps://dx.doi.org/10.1097/MNH.0b013e32834122f1
dc.identifier.urihttps://hdl.handle.net/20.500.12395/26636
dc.identifier.volume20en_US
dc.identifier.wosWOS:000285133300006en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherLIPPINCOTT WILLIAMS & WILKINSen_US
dc.relation.ispartofCURRENT OPINION IN NEPHROLOGY AND HYPERTENSIONen_US
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectarterial complianceen_US
dc.subjectdietary potassiumen_US
dc.subjectdietary sodiumen_US
dc.subjectnitric oxideen_US
dc.subjectTGF-betaen_US
dc.titleMechanisms and consequences of salt sensitivity and dietary salt intakeen_US
dc.typeReviewen_US

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