Mansley M, Neuhuber W, Korbmacher C, Bertog M (2015)
Publication Type: Journal article
Publication year: 2015
Publisher: American Physiological Society
Book Volume: 308
Pages Range: F450-8
Journal Issue: 5
DOI: 10.1152/ajprenal.00548.2014
There is good evidence for a causal link between excessive sympathetic drive to the kidney and hypertension. We hypothesized that sympathetic regulation of tubular Na(+) absorption may occur in the aldosterone-sensitive distal nephron, where the fine tuning of renal Na(+) excretion takes place. Here, the appropriate regulation of transepithelial Na(+) transport, mediated by the amiloride-sensitive epithelial Na(+) channel (ENaC), is critical for blood pressure control. To explore a possible effect of the sympathetic transmitter norepinephrine on ENaC-mediated Na(+) transport, we performed short-circuit current (Isc) measurements on confluent mCCDcl1 murine cortical collecting duct cells. Norepinephrine caused a complex Isc response with a sustained increase of amiloride-sensitive Isc by ~44%. This effect was concentration dependent and mediated via basolateral ?2-adrenoceptors. In cells pretreated with aldosterone, the stimulatory effect of norepinephrine was reduced. Finally, we demonstrated that noradrenergic nerve fibers are present in close proximity to ENaC-expressing cells in murine kidney slices. We conclude that the sustained stimulatory effect of locally elevated norepinephrine on ENaC-mediated Na(+) absorption may contribute to the hypertensive effect of increased renal sympathetic activity.
APA:
Mansley, M., Neuhuber, W., Korbmacher, C., & Bertog, M. (2015). Norepinephrine stimulates the epithelial Na+ channel in cortical collecting duct cells via ?2-adrenoceptors. American Journal of Physiology-Renal Physiology, 308(5), F450-8. https://doi.org/10.1152/ajprenal.00548.2014
MLA:
Mansley, Morag, et al. "Norepinephrine stimulates the epithelial Na+ channel in cortical collecting duct cells via ?2-adrenoceptors." American Journal of Physiology-Renal Physiology 308.5 (2015): F450-8.
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