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Endothelin type A a...
Endothelin type A and B receptors in the control of afferent and efferent arterioles in mice
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Schildroth, Janice (författare)
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Rettig-Zimmermann, Juliane (författare)
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Kalk, Philipp (författare)
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Steege, Andreas (författare)
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Faehling, Michael (författare)
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Sendeski, Mauricio (författare)
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Paliege, Alexander (författare)
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- Lai, En Yin (författare)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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Bachmann, Sebastian (författare)
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Persson, Pontus B. (författare)
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Hocher, Berthold (författare)
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Patzak, Andreas (författare)
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(creator_code:org_t)
- 2010-09-02
- 2011
- Engelska.
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Ingår i: Nephrology, Dialysis and Transplantation. - : Oxford University Press (OUP). - 0931-0509 .- 1460-2385. ; 26:3, s. 779-789
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- 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.
Nyckelord
- endothelin
- ETB receptor-deficient mouse
- glomerular arterioles
- renal haemodynamics
- MEDICINE
- MEDICIN
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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Till lärosätets databas
- Av författaren/redakt...
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Schildroth, Jani ...
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Rettig-Zimmerman ...
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Kalk, Philipp
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Steege, Andreas
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Faehling, Michae ...
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Sendeski, Mauric ...
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visa fler...
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Paliege, Alexand ...
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Lai, En Yin
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Bachmann, Sebast ...
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Persson, Pontus ...
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Hocher, Berthold
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Patzak, Andreas
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visa färre...
- Artiklar i publikationen
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Nephrology, Dial ...
- Av lärosätet
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Uppsala universitet