Redox regulation of ion channels in the pulmonary circulation.
CONCLUSIONS
The pulmonary circulation is a low-pressure, low-resistance, highly compliant vasculature. In contrast to the systemic circulation, it is not primarily regulated by a central nervous control mechanism. The regulation of resting membrane potential due to ion channels is of integral importance in the physiology and pathophysiology of the pulmonary vasculature.


BACKGROUND
Redox-driven ion conductance changes initiated by direct oxidation, nitration, and S-nitrosylation of the cysteine thiols and indirect phosphorylation of the threonine and serine residues directly affect pulmonary vascular tone.


RESULTS
Molecular mechanisms of changes in ion channel conductance, especially the identification of the sites of action, are still not fully elucidated.


CONCLUSIONS
Further investigation of the interaction between redox status and ion channel gating, especially the physiological significance of S-glutathionylation and S-nitrosylation, could result in a better understanding of the physiological and pathophysiological importance of these mediators in general and the implications of such modifications in cellular functions and related diseases and their importance for targeted treatment strategies.
1 Ludwig Boltzmann Institute for Lung Vascular Research , Graz, Austria .
Andrea
A
Olschewski
Edward Kenneth
EK
Weir
D002118:Calcium / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D015640:Ion Channel Gating; D007473:Ion Channels / Q000378:metabolism*; D009249:NADP / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D010084:Oxidation-Reduction; D011652:Pulmonary Circulation; D017382:Reactive Oxygen Species / Q000378:metabolism; D013879:Thioredoxins / Q000378:metabolism
D007473:Ion Channels; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D013879:Thioredoxins; D009249:NADP; D005978:Glutathione; D002118:Calcium