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Department of Internal Medicine, Department of Veterans Affairs Medical Center and University of Iowa College of Medicine, Iowa City, Iowa 52242
Stretching
the renal pelvic wall increases ipsilateral afferent renal nerve
activity (ARNA). This response is enhanced by inhibiting
Na+-K+-ATPase
with ouabain, suggesting a modulatory role for intracellular Na+ in the activation of
mechanosensitive neurons. The messenger RNA for 
-, 
-, and
-subunits of epithelial Na+
channels (ENaC) is found in collecting duct cells. Because ENaC subunits show homology with genes involved in mechanosensation, we
examined whether ENaC mRNA could be found in the pelvic wall and
whether the ARNA response to increased renal pelvic pressure was
modulated by blockers of the Na+
channel. -, -, and -subunits are present in the pelvis. The messenger RNA for the - and -subunits is readily detected by in
situ hybridization throughout the uroepithelium. The ARNA response to
increased renal pelvic pressure was reduced by 53 ± 10% and 40 ± 10% (P < 0.01) by renal
pelvic perfusion with the inhibitors amiloride and benzamil,
respectively. Amiloride inhibited the ouabain-induced enhancement of
the ARNA response to increased renal pelvic pressure. The magnitude of
this inhibition was inversely correlated with the magnitude of the
amiloride-mediated blockade of the ARNA response to increased renal
pelvic pressure (P < 0.001). Amiloride also reduced the ARNA response to renal pelvic administration of substance P, a mediator of the ARNA response to increased renal pelvic pressure. We conclude that the ENaC complex in the pelvic uroepithelium participates in the activation of renal pelvic
mechanosensitive neurons.
epithelial sodium channel; mechanosensitive nerves; afferent renal nerve activity; benzamil; renal pelvis; uroepithelium; substance P
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