Journal
PLOS ONE
Volume 13, Issue 2, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0193032
Keywords
-
Categories
Funding
- CIHR [M0P62931, M0P77756]
- E-Rare Joint Translational Call (JTC) for European Research Projects on Rare Diseases
- TF grant [016002]
- Danish Heart Association [13-04-1294-A4646-22776]
- Novo Nordisk Foundation [13273]
- Danish Council for Independent Research [DFF-1331-00086]
- Fabrikant Vilhelm Pedersen og Hustrus Mindelegat (on recommendation from the Novo Nordisk Foundation)
- Novo Nordisk Foundation
- Carlsberg Foundation
- A.P. Moller Foundation
- Beckett Foundation
- Helen AMP
- Ejnar Bjornows Foundation
- Lundbeck Foundation
- Astra Zeneca
Ask authors/readers for more resources
Aldosterone blockade confers substantial cardiovascular and renal protection. The effects of aldosterone on mineralocorticoid receptors (MR) expressed in endothelial cells (EC) within the renal vasculature have not been delineated. We hypothesized that lack of MR in EC may be protective in renal vasculature and examined this by ablating the Nr3c2 gene in endothelial cells (EC-MR) in mice. Blood pressure, heart rate and PAH clearance were measured using indwelling catheters in conscious mice. The role of the MR in EC on contraction and relaxation was investigated in the renal artery and in perfused afferent arterioles. Urinary sodium excretion was determined by use of metabolic cages. EC-MR transgenics had markedly decreased MR expression in isolated aortic endothelial cells as compared to litter-mates (WT). Blood pressure and effective renal plasma flow at baseline and following AngII infusion was similar between groups. No differences in contraction and relaxation were observed between WT and EC-MR KO in isolated renal arteries during baseline or following 2 or 4 weeks of AngII infusion. The constriction or dilatations of afferent arterioles between genotypes were not different. No changes were found between the groups with respect to urinary excretion of sodium after 4 weeks of AngII infusion, or in urinary albumin excretion and kidney morphology. In conclusion, deletion of the EC-MR does not confer protection towards the development of hypertension, endothelial dysfunction of renal arteries or renal function following prolonged AngII-infusion.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available