Document Detail

Angiotensin II regulation of renal vascular ENaC proteins.
MedLine Citation:
PMID:  19325536     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: The importance of beta and gamma epithelial Na(+) channel (ENaC) proteins in vascular smooth muscle cell (VSMC)-mediated pressure-induced constriction in renal interlobar arteries has been demonstrated recently. In renal epithelial tissue, ENaC expression is regulated by angiotensin II (Ang II). However, whether Ang II regulates vascular ENaC expression has never been determined. Therefore, the goal of the current investigation was to determine whether Ang II affects vascular ENaC expression and its contribution to pressure-induced constriction.
METHODS: To address this goal, Sprague-Dawley rats were infused with Ang II (50 ng/kg/min) via osmotic minipump for 1 week. Mean arterial pressure (MAP) was measured using radiotelemetry. Interlobar arteries were isolated from these animals to assess VSMC ENaC protein expression, pressure-induced constriction, and agonist induced vascular reactivity.
RESULTS: MAP was not different in control (113 +/- 2 mm Hg) and Ang II- (114 +/- 2 mm Hg) infused mice. We found that Ang II infusion decreased renal VSMC beta and gammaENaC immunolabeling by 18%. Consistent with this finding, we also found that ENaC-dependent peak pressure-induced constriction was inhibited from 38 +/- 3% to 25 +/- 1% at 125 mm Hg. Vasoreactivity to KCl, phenylephrine (PE), and acetylcholine (ACh) was unchanged.
CONCLUSIONS: Ang II suppression of pressure-induced constrictor responses in renal interlobar arteries may be mediated, at least in part, by inhibition of beta and gammaENaC protein expression.
Nikki L Jernigan; Joshua Speed; Babette LaMarca; Joey P Granger; Heather A Drummond
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2009-03-26
Journal Detail:
Title:  American journal of hypertension     Volume:  22     ISSN:  1941-7225     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-05-20     Completed Date:  2009-06-23     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  United States    
Other Details:
Languages:  eng     Pagination:  593-7     Citation Subset:  IM    
Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, USA.
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MeSH Terms
Angiotensin II / administration & dosage*
Blood Pressure / drug effects
Disease Models, Animal
Epithelial Sodium Channel / biosynthesis*,  drug effects
Hypertension, Renovascular / metabolism*,  physiopathology
Infusions, Intravenous
Muscle, Smooth, Vascular / drug effects,  metabolism*
Rats, Sprague-Dawley
Renal Artery / drug effects,  metabolism*,  physiopathology
Vasoconstriction / physiology
Vasoconstrictor Agents / administration & dosage*
Grant Support
Reg. No./Substance:
0/Epithelial Sodium Channel; 0/Vasoconstrictor Agents; 11128-99-7/Angiotensin II

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