Journal Article

Endothelin type A and B receptors in the control of afferent and efferent arterioles in mice

Janice Schildroth, Juliane Rettig-Zimmermann, Philipp Kalk, Andreas Steege, Michael Fähling, Mauricio Sendeski, Alexander Paliege, En Yin Lai, Sebastian Bachmann, Pontus B. Persson, Berthold Hocher and Andreas Patzak

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 26, issue 3, pages 779-789
Published in print March 2011 | ISSN: 0931-0509
Published online September 2010 | e-ISSN: 1460-2385 | DOI:
Endothelin type A and B receptors in the control of afferent and efferent arterioles in mice

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Background. Endothelin 1 contributes to renal blood flow control and pathogenesis of kidney diseases. The differential effects, however, of endothelin 1 (ET-1) on afferent (AA) and efferent arterioles (EA) remain to be established.

Methods. We investigated endothelin type A and B receptor (ETA-R, ETB-R) functions in the control of AA and EA. Arterioles of ETB-R deficient, rescued mice [ETB(−/−)] and wild types [ETB(+/+)] were microperfused.

Results. ET-1 constricted AA stronger than EA in ETB(−/−) and ETB(+/+) mice. Results in AA: ET-1 induced similar constrictions in ETB(−/−) and ETB(+/+) mice. BQ-123 (ETA-R antagonist) inhibited this response in both groups. ALA-ET-1 and IRL1620 (ETB-R agonists) had no effect on arteriolar diameter. L-NAME did neither affect basal diameters nor ET-1 responses. Results in EA: ET-1 constricted EA stronger in ETB(+/+) compared to ETB(−/−). BQ-123 inhibited the constriction completely only in ETB(−/−). ALA-ET-1 and IRL1620 constricted only arterioles of ETB(+/+) mice. L-NAME decreased basal diameter in ETB(+/+), but not in ETB(−/−) mice and increased the ET-1 response similarly in both groups. The L-NAME actions indicate a contribution of ETB-R in basal nitric oxide (NO) release in EA and suggest dilatory action of ETA-R in EA.

Conclusions. ETA-R mediates vasoconstriction in AA and contributes to vasoconstriction in EA in this mouse model. ETB-R has no effect in AA but mediates basal NO release and constriction in EA. The stronger effect of ET-1 on AA supports observations of decreased glomerular filtration rate to ET-1 and indicates a potential contribution of ET-1 to the pathogenesis of kidney diseases.

Keywords: endothelin; ETB receptor-deficient mouse; glomerular arterioles; renal haemodynamics

Journal Article.  5382 words.  Illustrated.

Subjects: Nephrology

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