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. 2017 Aug 4;7:7264. doi: 10.1038/s41598-017-07585-y

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Model for the role of the AE3 Cl⁻/HCO₃ ⁻ exchanger in transport-mediated CO₂ disposal. Oxygen entering the myocyte is rapidly converted to CO₂ in mitochondria. CO₂ venting from mitochondria¹³ is facilitated by CA-mediated conversion of CO₂ to HCO₃ ⁻ and H⁺, with H⁺ buffered by histidyl dipeptides (HDP) and other components, thereby effectively blocking the back reaction by keeping the concentration of free H⁺ low. CO₂ disposal is proposed to be mediated by a combination of HCO₃ ⁻ extrusion by AE3, Cl⁻ recycling via Cl⁻ channel activity, H⁺-extrusion via HVCN1 during each depolarization, and extracellular carbonic anhydrase (CA) activity to generate CO₂.