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Conceived and designed the experiments: RLS SMW. Performed the experiments: RLS ERW YHK LAW AME-A JM RB SR JWV LH TDP SH VP. Analyzed the data: RLS LAW RB DCE JWV LH RLG SMW. Wrote the paper: RLS SMW.

We thank Drs. C. Subah Packer, W. Charles O'Neill, Richard J. Paul, Kathy Griendling, David G. Harrison and L. Gabriel Navar for their helpful suggestions.

The authors have declared that no competing interests exist.


Research Funding:

Funding provided by National Institute of Diabetes, Digestive and Kidney Diseases grants 46493 (to S. M. Wall); 37963 (to D. C. Eaton); and National Heart, Lung and Blood Institute grant 070892 (to R. L. Sutliff).

The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.


  • Science & Technology
  • Multidisciplinary Sciences
  • Science & Technology - Other Topics
  • C57BL/6J MOUSE

Contractile Force Is Enhanced in Aortas from Pendrin Null Mice Due to Stimulation of Angiotensin II-Dependent Signaling

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Journal Title:



Volume 9, Number 8


, Pages e105101-e105101

Type of Work:

Article | Final Publisher PDF


Pendrin is a Cl-/HCO3- exchanger expressed in the apical regions of renal intercalated cells. Following pendrin gene ablation, blood pressure falls, in part, from reduced renal NaCl absorption. We asked if pendrin is expressed in vascular tissue and if the lower blood pressure observed in pendrin null mice is accompanied by reduced vascular reactivity. Thus, the contractile responses to KCl and phenylephrine (PE) were examined in isometrically mounted thoracic aortas from wild-type and pendrin null mice. Although pendrin expression was not detected in the aorta, pendrin gene ablation changed contractile protein abundance and increased the maximal contractile response to PE when normalized to cross sectional area (CSA). However, the contractile sensitivity to this agent was unchanged. The increase in contractile force/cross sectional area observed in pendrin null mice was due to reduced cross sectional area of the aorta and not from increased contractile force per vessel. The pendrin-dependent increase in maximal contractile response was endothelium- and nitric oxide-independent and did not occur from changes in Ca2+ sensitivity or chronic changes in catecholamine production. However, application of 100 nM angiotensin II increased force/CSA more in aortas from pendrin null than from wild type mice. Moreover, angiotensin type 1 receptor inhibitor (candesartan) treatment in vivo eliminated the pendrin-dependent changes contractile protein abundance and changes in the contractile force/cross sectional area in response to PE. In conclusion, pendrin gene ablation increases aorta contractile force per cross sectional area in response to angiotensin II and PE due to stimulation of angiotensin type 1 receptor-dependent signaling. The angiotensin type 1 receptor-dependent increase in vascular reactivity may mitigate the fall in blood pressure observed with pendrin gene ablation.

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© 2014 Sutliff et al.

This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits distribution of derivative works, making multiple copies, distribution, public display, and publicly performance, provided the original work is properly cited. This license requires credit be given to copyright holder and/or author, copyright and license notices be kept intact.

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