BioMed Research International
Volume 2018 (2018), Article ID 3081532, 2 pages
https://doi.org/10.1155/2018/3081532

Erratum

Erratum to “Contribution of Ca²⁺-Dependent Cl⁻ Channels to Norepinephrine-Induced Contraction of Femoral Artery Is Replaced by Increasing EDCF Contribution during Ageing”

Silvia Liskova,1,2 Miriam Petrova,² Petr Karen,¹ Michal Behuliak,¹ and Josef Zicha¹

¹Institute of Physiology, Academy of Sciences of the Czech Republic, 14220 Prague 4, Czech Republic
²Institute of Pharmacology, Faculty of Medicine, Comenius University, Bratislava, Slovakia

Correspondence should be addressed to Silvia Liskova; silvia.liskova@gmail.com

Received 27 December 2017; Accepted 1 January 2018; Published 20 February 2018

Copyright © 2018 Silvia Liskova et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

In the article titled “Contribution of Ca²⁺-Dependent Cl⁻ Channels to Norepinephrine-Induced Contraction of Femoral Artery Is Replaced by Increasing EDCF Contribution during Ageing” [1], there was an error in the key of Figure 2, which is corrected as follows.

Figure 2: Norepinephrine concentration-response curves obtained in femoral arteries of 20-month-old WKY rats (WKY) recorded under the control conditions and after Ca²⁺-dependent Cl⁻ channels blockade (R(+)-IAA-94, IAA) or after the inhibition of cyclooxygenase (indomethacin, IME) or in the presence of niflumic acid (NIFLU). Data are presented as mean ± SEM (for number of vessels see Table ). Depicted curves were calculated from average values obtained at studied norepinephrine concentrations.

References

S. Liskova, M. Petrova, P. Karen, M. Behuliak, and J. Zicha, “Contribution of Ca²⁺-dependent Cl⁻ channels to norepinephrine-induced contraction of femoral artery is replaced by increasing EDCF contribution during ageing,” BioMed Research International, vol. 2014, Article ID 289361, 9 pages, 2014.