Research ExplorerPublicationsDeoxycorticosterone Acetate/Salt-Induced Cardiac But Not Ren...

Deoxycorticosterone Acetate/Salt-Induced Cardiac But Not Renal Injury Is Mediated By Endothelial Mineralocorticoid Receptors Independently From Blood Pressure

Standard

Deoxycorticosterone Acetate/Salt-Induced Cardiac But Not Renal Injury Is Mediated By Endothelial Mineralocorticoid Receptors Independently From Blood Pressure. / Lother, Achim; Fürst, David; Bergemann, Stella; Gilsbach, Ralf; Grahammer, Florian; Huber, Tobias B; Hilgendorf, Ingo; Bode, Christoph; Moser, Martin; Hein, Lutz.

In: HYPERTENSION, Vol. 67, No. 1, 01.2016, p. 130-8.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Lother, A, Fürst, D, Bergemann, S, Gilsbach, R, Grahammer, F, Huber, TB, Hilgendorf, I, Bode, C, Moser, M & Hein, L 2016, 'Deoxycorticosterone Acetate/Salt-Induced Cardiac But Not Renal Injury Is Mediated By Endothelial Mineralocorticoid Receptors Independently From Blood Pressure', HYPERTENSION, vol. 67, no. 1, pp. 130-8. https://doi.org/10.1161/HYPERTENSIONAHA.115.06530

APA

Lother, A., Fürst, D., Bergemann, S., Gilsbach, R., Grahammer, F., Huber, T. B., Hilgendorf, I., Bode, C., Moser, M., & Hein, L. (2016). Deoxycorticosterone Acetate/Salt-Induced Cardiac But Not Renal Injury Is Mediated By Endothelial Mineralocorticoid Receptors Independently From Blood Pressure. HYPERTENSION, 67(1), 130-8. https://doi.org/10.1161/HYPERTENSIONAHA.115.06530

Vancouver

Lother A, Fürst D, Bergemann S, Gilsbach R, Grahammer F, Huber TB et al. Deoxycorticosterone Acetate/Salt-Induced Cardiac But Not Renal Injury Is Mediated By Endothelial Mineralocorticoid Receptors Independently From Blood Pressure. HYPERTENSION. 2016 Jan;67(1):130-8. https://doi.org/10.1161/HYPERTENSIONAHA.115.06530

Bibtex

@article{75a06d39aa304f3c9166a3f9fadd16cc,
title = "Deoxycorticosterone Acetate/Salt-Induced Cardiac But Not Renal Injury Is Mediated By Endothelial Mineralocorticoid Receptors Independently From Blood Pressure",
abstract = "Chronic kidney disease has a tremendously increasing prevalence and requires novel therapeutic approaches. Mineralocorticoid receptor (MR) antagonists have proven highly beneficial in the therapy of cardiac disease. The cellular and molecular events leading to cardiac inflammation and remodeling are proposed to be similar to those mediating renal injury. Thus, this study was designed to evaluate and directly compare the effect of MR deletion in endothelial cells on cardiac and renal injury in a model of deoxycorticosterone acetate-induced hypertension. Endothelial MR deletion ameliorated deoxycorticosterone acetate/salt-induced cardiac remodeling. This was associated with a reduced expression of the vascular cell adhesion molecule Vcam1 in MR-deficient cardiac endothelial cells. Ambulatory blood pressure telemetry revealed that the protective effect of MR deletion was independent from blood pressure. Similar to the heart, deoxycorticosterone acetate/salt-induced severe renal injury, including inflammation, fibrosis, glomerular injury, and proteinuria. However, no differences in renal injury were observed between genotypes. In conclusion, MR deletion from endothelial cells ameliorated deoxycorticosterone acetate/salt-induced cardiac inflammation and remodeling independently from alterations in blood pressure but it did not affect renal injury. These findings suggest that the anti-inflammatory mechanism mediating organ protection after endothelial cell MR deletion is specific for the heart versus the kidney.",
keywords = "Animals, Blood Pressure, Cells, Cultured, Desoxycorticosterone Acetate, Disease Models, Animal, Endothelium, Vascular, Gene Expression Regulation, Hypertension, Immunohistochemistry, Kidney, Male, Mice, Mice, Mutant Strains, Polymerase Chain Reaction, RNA, Receptors, Mineralocorticoid, Vascular Cell Adhesion Molecule-1, Ventricular Remodeling, Journal Article, Research Support, Non-U.S. Gov't",
author = "Achim Lother and David F{\"u}rst and Stella Bergemann and Ralf Gilsbach and Florian Grahammer and Huber, {Tobias B} and Ingo Hilgendorf and Christoph Bode and Martin Moser and Lutz Hein",
note = "{\textcopyright} 2015 American Heart Association, Inc.",
year = "2016",
month = jan,
doi = "10.1161/HYPERTENSIONAHA.115.06530",
language = "English",
volume = "67",
pages = "130--8",
journal = "HYPERTENSION",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

RIS

TY - JOUR

T1 - Deoxycorticosterone Acetate/Salt-Induced Cardiac But Not Renal Injury Is Mediated By Endothelial Mineralocorticoid Receptors Independently From Blood Pressure

AU - Lother, Achim

AU - Fürst, David

AU - Bergemann, Stella

AU - Gilsbach, Ralf

AU - Grahammer, Florian

AU - Huber, Tobias B

AU - Hilgendorf, Ingo

AU - Bode, Christoph

AU - Moser, Martin

AU - Hein, Lutz

N1 - © 2015 American Heart Association, Inc.

PY - 2016/1

Y1 - 2016/1

N2 - Chronic kidney disease has a tremendously increasing prevalence and requires novel therapeutic approaches. Mineralocorticoid receptor (MR) antagonists have proven highly beneficial in the therapy of cardiac disease. The cellular and molecular events leading to cardiac inflammation and remodeling are proposed to be similar to those mediating renal injury. Thus, this study was designed to evaluate and directly compare the effect of MR deletion in endothelial cells on cardiac and renal injury in a model of deoxycorticosterone acetate-induced hypertension. Endothelial MR deletion ameliorated deoxycorticosterone acetate/salt-induced cardiac remodeling. This was associated with a reduced expression of the vascular cell adhesion molecule Vcam1 in MR-deficient cardiac endothelial cells. Ambulatory blood pressure telemetry revealed that the protective effect of MR deletion was independent from blood pressure. Similar to the heart, deoxycorticosterone acetate/salt-induced severe renal injury, including inflammation, fibrosis, glomerular injury, and proteinuria. However, no differences in renal injury were observed between genotypes. In conclusion, MR deletion from endothelial cells ameliorated deoxycorticosterone acetate/salt-induced cardiac inflammation and remodeling independently from alterations in blood pressure but it did not affect renal injury. These findings suggest that the anti-inflammatory mechanism mediating organ protection after endothelial cell MR deletion is specific for the heart versus the kidney.

AB - Chronic kidney disease has a tremendously increasing prevalence and requires novel therapeutic approaches. Mineralocorticoid receptor (MR) antagonists have proven highly beneficial in the therapy of cardiac disease. The cellular and molecular events leading to cardiac inflammation and remodeling are proposed to be similar to those mediating renal injury. Thus, this study was designed to evaluate and directly compare the effect of MR deletion in endothelial cells on cardiac and renal injury in a model of deoxycorticosterone acetate-induced hypertension. Endothelial MR deletion ameliorated deoxycorticosterone acetate/salt-induced cardiac remodeling. This was associated with a reduced expression of the vascular cell adhesion molecule Vcam1 in MR-deficient cardiac endothelial cells. Ambulatory blood pressure telemetry revealed that the protective effect of MR deletion was independent from blood pressure. Similar to the heart, deoxycorticosterone acetate/salt-induced severe renal injury, including inflammation, fibrosis, glomerular injury, and proteinuria. However, no differences in renal injury were observed between genotypes. In conclusion, MR deletion from endothelial cells ameliorated deoxycorticosterone acetate/salt-induced cardiac inflammation and remodeling independently from alterations in blood pressure but it did not affect renal injury. These findings suggest that the anti-inflammatory mechanism mediating organ protection after endothelial cell MR deletion is specific for the heart versus the kidney.

KW - Animals

KW - Blood Pressure

KW - Cells, Cultured

KW - Desoxycorticosterone Acetate

KW - Disease Models, Animal

KW - Endothelium, Vascular

KW - Gene Expression Regulation

KW - Hypertension

KW - Immunohistochemistry

KW - Kidney

KW - Male

KW - Mice

KW - Mice, Mutant Strains

KW - Polymerase Chain Reaction

KW - RNA

KW - Receptors, Mineralocorticoid

KW - Vascular Cell Adhesion Molecule-1

KW - Ventricular Remodeling

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1161/HYPERTENSIONAHA.115.06530

DO - 10.1161/HYPERTENSIONAHA.115.06530

M3 - SCORING: Journal article

C2 - 26553231

VL - 67

SP - 130

EP - 138

JO - HYPERTENSION

JF - HYPERTENSION

SN - 0194-911X

IS - 1

ER -