Impaired myogenic constriction of the renal afferent arteriole in a mouse model of reduced ßENaC expression.
Am J Physiol Renal Physiol
; 302(11): F1486-93, 2012 Jun 01.
Article
em En
| MEDLINE
| ID: mdl-22419697
ABSTRACT
Previous studies demonstrate a role for ß epithelial Na(+) channel (ßENaC) protein as a mediator of myogenic constriction in renal interlobar arteries. However, the importance of ßENaC as a mediator of myogenic constriction in renal afferent arterioles, the primary site of development of renal vascular resistance, has not been determined. We colocalized ßENaC with smooth muscle α-actin in vascular smooth muscle cells in renal arterioles using immunofluorescence. To determine the importance of ßENaC in myogenic constriction in renal afferent arterioles, we used a mouse model of reduced ßENaC (ßENaC m/m) and examined pressure-induced constrictor responses in the isolated afferent arteriole-attached glomerulus preparation. We found that, in response to a step increase in perfusion pressure from 60 to 120 mmHg, the myogenic tone increased from 4.5 ± 3.7 to 27.3 ± 5.2% in +/+ mice. In contrast, myogenic tone failed to increase with the pressure step in m/m mice (3.9 ± 0.8 to 6.9 ± 1.4%). To determine the importance of ßENaC in myogenic renal blood flow (RBF) regulation, we examined the rate of change in renal vascular resistance following a step increase in perfusion pressure in volume-expanded animals. We found that, following a step increase in pressure, the rate of myogenic correction of RBF is inhibited by 75% in ßENaC m/m mice. These findings demonstrate that myogenic constriction in afferent arterioles is dependent on normal expression of ßENaC.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Arteríolas
/
Circulação Renal
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Canais Epiteliais de Sódio
/
Músculo Liso Vascular
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2012
Tipo de documento:
Article