Aldosterone synthase knockout mouse as a model for sodium-induced endothelial sodium channel up-regulation in vascular endothelium

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
Pia JeggleKristina Kusche-Vihrog

Abstract

Recently, a novel feedforward activation of the endothelial epithelial sodium channel (ENaC) [endothelial sodium channel (EnNaC)] by sodium was reported that counteracts ENaC function in kidney. In the absence of aldosterone, a rise in extracellular sodium (>145 mM) increases EnNaC surface abundance, thereby stiffening the cortex of vascular endothelial cells (ECs) in vitro. The latter reduces the release of NO-the hallmark of endothelial dysfunction. Here, we test whether high extracellular sodium per se increases EnNaC expression and cortical stiffness in an aldosterone synthase (Cyp11b2)-deficient (AS(-/-)) mouse model. Therefore, we employed in situ ECs of ex vivo aorta preparations from wild-type (WT) and AS(-/-). EnNaC surface expression (-16%) and cortical stiffness (-22%) were reduced in AS(-/-), compared with WT, whereas NO secretion was exclusively detectable in AS(-/-). EnNaC inhibition with benzamil decreased stiffness in both, while mineralocorticoid receptor antagonism diminished stiffness only in the WT. In the absence of aldosterone, high sodium (150 mM) increased EnNaC surface expression ex vivo (plus 19%) and cortical stiffness ex vivo (plus 41%) and in vivo (plus 44%). Application of aldosterone adjusted the ...Continue Reading

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Citations

Jan 27, 2018·American Journal of Physiology. Heart and Circulatory Physiology·Zoe AshleyMartin Fronius
Apr 14, 2017·Scientific Reports·Florian SchierkeKristina Kusche-Vihrog
Feb 13, 2018·Antioxidants & Redox Signaling·Johannes Fels, Kristina Kusche-Vihrog
Jul 28, 2020·Cardiovascular Research·Eva Roy-ChowdhurySibylle von Vietinghoff

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