Angiotensin II regulation of renal vascular ENaC proteins.
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.
Jernigan
Nikki L
NL
Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Speed
Joshua
J
LaMarca
Babette
B
Granger
Joey P
JP
Drummond
Heather A
HA