| First Author | Ge Y | Year | 2012 |
| Journal | Am J Physiol Renal Physiol | Volume | 302 |
| Issue | 11 | Pages | F1486-93 |
| PubMed ID | 22419697 | Mgi Jnum | J:185461 |
| Mgi Id | MGI:5428812 | Doi | 10.1152/ajprenal.00638.2011 |
| Citation | Ge Y, et al. (2012) Impaired myogenic constriction of the renal afferent arteriole in a mouse model of reduced betaENaC expression. Am J Physiol Renal Physiol 302(11):F1486-93 |
| abstractText | Previous studies demonstrate a role for beta epithelial Na(+) channel (betaENaC) protein as a mediator of myogenic constriction in renal interlobar arteries. However, the importance of betaENaC 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 betaENaC with smooth muscle alpha-actin in vascular smooth muscle cells in renal arterioles using immunofluorescence. To determine the importance of betaENaC in myogenic constriction in renal afferent arterioles, we used a mouse model of reduced betaENaC (betaENaC 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 betaENaC 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 betaENaC m/m mice. These findings demonstrate that myogenic constriction in afferent arterioles is dependent on normal expression of betaENaC. |
