![]() ![]() 2009) and rhesus proteins (Endeward et al. ![]() However, this view has been challenged with the discovery of the effect of cholesterol on CO 2 permeability and of protein channels used by CO 2 to cross membranes, aquaporins (AQPs) (Verkman, 2007 Musa‐Aziz et al. Here, we review recent advances in our understanding of the effects of hypercapnia on the lung.ĬO 2 is a small non‐polar molecule thought to traverse biological cell membranes via passive diffusion, depending upon the transmembrane concentration gradient of CO 2 and the lipid/water partition behaviour of the gas (Missner & Pohl, 2009). ![]() Despite the fact that the lung is the primary site of CO 2 elimination, the effects of hypercapnia have been argued and contradictory data have been reported. In humans, elevated CO 2 (hypercapnia) can occur as a consequence of lung diseases when inadequate gas exchange takes place (Vadasz et al. 2014) and inextricably linked to physiological conditions. The physiological levels of CO 2 in exhaled breath of mammals are significantly higher than the room air (∼5% vs. Abbreviations ALI acute lung injury AMPK AMP kinase AQP aquaporin ARDS acute respiratory distress syndrome cAMP 3′,5′‐cyclic adenosine monophosphate CAMKK‐β Ca 2+/calmodulin‐dependent protein kinase kinase‐β COPD chronic obstructive pulmonary disease ERK extracellular signal‐regulated kinase IL‐6 interleukin‐6 IDH2, isocitrate dehydrogenase‐2 JNK c‐Jun‐N‐terminal kinase PAL prolonged air leak PKA‐Iα, protein kinase A‐Iα PKC‐ζ protein kinase C‐ζ sAC soluble adenylyl cyclase TNF tumour necrosis factorIntroductionĬarbon dioxide (CO 2) is a primary product of oxidative metabolism. ![]()
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