NDLI: Transforming growth factor-ß mediates endothelial dysfunction in rats during high salt intake.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Feng, Wenguang Ying, Wei-Zhong Aaron, Kristal J. Sanders, Paul W.
Description	Author Affiliation: Feng W ( Division of Nephrology, Department of Medicine, Nephrology Research and Training Center, University of Alabama at Birmingham, Birmingham, Alabama); Ying WZ ( Division of Nephrology, Department of Medicine, Nephrology Research and Training Center, University of Alabama at Birmingham, Birmingham, Alabama); Aaron KJ ( Division of Nephrology, Department of Medicine, Nephrology Research and Training Center, University of Alabama at Birmingham, Birmingham, Alabama); Sanders PW ( Division of Nephrology, Department of Medicine, Nephrology Research and Training Center, University of Alabama at Birmingham, Birmingham, Alabama)
Abstract	Endothelial dysfunction has been shown to be predictive of subsequent cardiovascular events and death. Through a mechanism that is incompletely understood, increased dietary salt intake promotes endothelial dysfunction in healthy, salt-resistant humans. The present study tested the hypothesis that dietary salt-induced transforming growth factor (TGF)-ß promoted endothelial dysfunction and salt-dependent changes in blood pressure (BP). Sprague-Dawley rats that received diets containing 0.3% NaCl [low salt (LS)] or 8.0% NaCl [high salt (HS)] were treated with vehicle or SB-525334, a specific inhibitor of TGF-ß receptor I/activin receptor-like kinase 5, beginning on day 5. BP was monitored using radiotelemetry in four groups of rats (LS, LS + SB-525334, HS, and HS + SB-525334) for up to 14 days. By day 14 of the study, mean daytime systolic BP and mean pulse pressure of the HS group treated with vehicle was greater than those in the other three groups; mean daytime systolic BP and pulse pressure of the HS + SB-525334 group did not differ from the LS and LS + SB-525334-treated groups. Whereas mean systolic BP, mean diastolic BP, and mean arterial pressure did not differ among the groups on the seventh day of the study, endothelium-dependent vasorelaxation was impaired specifically in the HS group; treatment with the activin receptor-like kinase 5 inhibitor prevented the dietary HS intake-induced increases in phospho-Smad2 (Ser(465/467)) and NADPH oxidase-4 in endothelial lysates and normalized endothelial function. These findings suggest that HS-induced endothelial dysfunction and the development of salt-dependent increases in BP were related to endothelial TGF-ß signaling.
File Format	HTM / HTML
ISSN	1931857X
Issue Number	12
Volume Number	309
e-ISSN	15221466
Journal	AJP: Renal Physiology
Language	English
Publisher	American Physiological Society
Publisher Date	2015-12-15
Publisher Place	United States
Access Restriction	Subscribed
Subject Keyword	Hypertension Blood Pressure Research Support, N.i.h., Extramural Heart Rate Eating Research Support, Non-u.s. Gov't Sodium Chloride Rats, Sprague-dawley Discipline Nephrology Male Protein-serine-threonine Kinases Pharmacology Metabolism Drug Effects Vasodilation Journal Article Endothelium Transforming Growth Factor Beta Physiopathology Discipline Physiology Animals Receptors, Transforming Growth Factor Beta Physiology Animal Feed
Content Type	Text
Resource Type	Article
Subject	Physiology Urology

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