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. 2018 Jun 19;9:753. doi: 10.3389/fphys.2018.00753

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Copyright © 2018 Mader, Müller, Krause, Springer, Kernig, Protzel, Porath, Rackow, Wittstock, Frank, Hakenberg, Köhling and Kirschstein.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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HCN1 contributes to the ZD7288-induced enhancement of phasic contractions. (A) Sample force recording showing the carbachol (CCh) and ZD7288-evoked response in a mouse bladder specimen. (B) Sample trace showing that pre-treatment with 18β-GA largely inhibited the ZD7288-induced tonic contraction as well as the enhancement of phasic contractions. (C) Tonic contractions by ZD7288 were not different between HCN1-deficient mice and wildtype littermates. (D) ZD7288 significantly enhanced phasic contraction amplitudes in both HCN1-knockout mice and controls (P < 0.001, Wilcoxon signed rank test). However, this increase was significantly more pronounced in HCN1-deficient mice (P < 0.05, Mann–Whitney test). Note that phasic contraction amplitudes were significantly higher in HCN1-knockout mice under baseline conditions (i.e., before ZD7288 application, P < 0.01, Mann–Whitney U-test). (E) Tonic contractions were significantly reduced by 18β-GA (P < 0.001, Mann–Whitney U-test), but without differences between HCN1^+/+ and HCN1^-/- genotypes. (F) The ZD7288-induced enhancement of phasic contractions was significantly sensitive to 18β-GA, again similar in both genotypes.