Objective:

Gap junctions are required for propagation of electromechanical activity in the renal pelvis. Renal denervation increases diuresis and renal pelvic contraction frequency. We investigated renal pelvic Cx expression and its dependence on renal innervation. Furthermore, we tested the effect of gap junction blockade on spontaneous and norepinephrine-induced renal pelvic contractions.

Methods:

Expression of Cx26, 36, 37, 40, 43 and 45 mRNA in human and rat renal pelvises was determined by real time RT-PCR. Protein expression of the Cx isoforms with the highest mRNA abundance was analysed by Western blot. Influence of renal innervation on Cx expression was tested on the mRNA level in renal pelvises from rat kidney transplants. The role of gap junctions for pelvic contractile activity was investigated in vitro by wire myography using the non-selective gap junction blocker 18β-glycyrrhetinic acid (18β-GA).

Results:

Cx40, Cx 43 and Cx45 mRNA were highly abundant in rat and human renal pelvises, which was confirmed on the protein level by Western blot analyses. Cx 40, 43 and 45 mRNA were reduced in denervated renal pelvises by 60, 30 and 50%, respectively, compared to innervated controls. 18β-GA did not significantly affect spontaneous contractions but significantly reduced the amplitude of norepinephrine-induced contractions in native rat renal pelvises.

Conclusions:

Cx 40, 43 and 45 are highly abundant in the renal pelvis and their expression depends on renal innervation. Renal innervation may contribute to chronic regulation of renal pelvic electromechanical activity including changes in gap junction-dependent propagation of electrical activity.