| Title | Altered whole kidney blood flow autoregulation in a mouse model of reduced {beta}ENaC. | | Author(s) | Grifoni SC, Chiposi R, McKey SE, Ryan MJ, Drummond HA | | Institution | University of Mississippi Medical Center. | | Source | Am J Physiol Renal Physiol 2009 Nov 4. | | Abstract | Renal blood flow (RBF) autoregulation is mediated by at least two mechanisms, the fast acting myogenic response (~5 s) and slow acting tubuloglomerular feedback (TGF, ~25 s). Previous studies suggest Epithelial Na(+) Channel (ENaC) family proteins, betaENaC in particular, mediate myogenic constriction in isolated renal interlobar arteries. However, it is unknown if betaENaC mediated myogenic constriction contributes to RBF autoregulation in vivo. Therefore, the goal of this investigation was to determine if the myogenic mediated RBF autoregulation is inhibited in a mouse model of reduced betaENaC (m/m). To address this goal, we evaluated the temporal response of RBF and renal vascular resistance (RVR) to a 2-minute step increase in mean arterial pressure (MAP). Pressure-induced changes in RBF and RVR at 0-5, 6-25 and 110-120 sec after step increase in MAP were used to assess the contribution of myogenic and TGF mechanisms and steady state autoregulation, respectively. The rate of the initial increase in RVR, attributed to the myogenic mechanism, was reduced by ~50% in m/m mice, indicating the speed of the myogenic response was inhibited. Steady state autoregulation was similar between betaENaC +/+ and m/m mice. Although the rate of the secondary increase in RVR, attributed to TGF, was similar in betaENaC +/+ and m/m mice, however, occurred over a longer period (+10 s), which may have allowed TGF to compensate for a loss in myogenic autoregulation. Our findings suggest betaENaC is an important mediator of renal myogenic constriction mediated RBF autoregulation in-vivo. Key words: autoregulation, Epithlelial Na+ Channel, renal blood flow, mechanotransduction. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19889952 |
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