Regulation of K+ Currents by CO in Carotid Body type I Cells and Pulmonary Artery Smooth Muscle Cells
Potassium channels are a diverse group of proteins that control membrane excitability and their regulation can influence cell signalling through the modulation of calcium entry. A subset of these channels appears to be particularly sensitive to oxygen tension and these play an important role in the regulation of arterial blood gas tensions. In pulmonary arterial smooth muscle cells, K+ channel activity is linked to contractile tone. Factors that regulate the activity of these channels therefore have a major influence upon blood vessel diameter and therefore on pulmonary artery (PA) blood pressure, thus altering regional ventilation -perfusion ratios in the lung. In carotid body (CB) type I cells, K+ channel activity is linked to the secretion of a variety of putative neurotransmitter and regulation of these channels therefore influences carotid sinus nerve activity and thus cardiorespiratory control. In both systems, hypoxia decreases the activity of a variety of K+ channels, some of which regulate the resting membrane potential. In CB type I cells and in PA smooth muscle cells, hypoxia decreases the activity of the TASK-1 channel (a background K+ channels in type one cells and probably KN channels in PA (Gurney et al.2002)), large conductance Ca2+-activated (BKca) channels and/or voltage-activated (Kv) channels depending on species and experimental conditions (Lopez-Barneo et al.2001).
KeywordsCarotid Body Rest Membrane Potential Chronic Hypoxia BKca Channel Hypoxic Pulmonary Vasoconstriction
Unable to display preview. Download preview PDF.
- Barbe, C, Al-Hashem, F., Conway, A.F., Dubuis, E., Vandier, C, and Kumar, P., 2001, Effect of carbon monoxide on whole cell currents of the isolated rat carotid body type I cell.J Physiol 533: 108P–109P.Google Scholar
- Conway, A.F., Pepper, D.R., and Kumar, P., 1997, Dose-dependent modulation of carotid body C02–02 interaction by carbon monoxide. J Physiol 504: 201P–202P.Google Scholar
- Dubuis, E., Gautier, M., Melin, A., Rebocho, M., Girardin, C, Bonnet, P., and Vandier, C, 2002, Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells. Am J Physiol Lung Cell Mol Physiol 283: L120–9.Google Scholar
- Joels, N., and Neil, E., 1962, The action of high tensions of carbon monoxide on the carotid chemoreceptors. Archives Internationales de Pharmacodynamic et de Thérapie 139: 528–534.Google Scholar
- Lloyd, B.B., Cunningham, D.J.C., Goode, R.C., Joels, N., and Neil, E., 1968, Depression of hypoxic hyperventilation in man by sudden inspiration of carbon monoxide. In Arterial Chemoreceptors (R. W.. Torrance, eds), Blackwell, Oxford, pp. 145–148.Google Scholar
- Minamino, T., Christou, H., Hsieh, CM., Liu, Y., Dhawan, V., Abraham, N.G., Perrella, M.A., Mitsialis, S.A., and Kourembanas, S., 2001, Targeted expression of heme oxygenase-1 prevents the pulmonary inflammatory and vascular responses to hypoxia. Proc Natl AcadSci USA 98: 8798–803.CrossRefGoogle Scholar
- Osipenko, O.N., Alexander, D., MacLean, M.R., and Gurney, A.M., 1998, Influence of chronic hypoxia on the contributions of non-inactivating and delayed rectifier K currents to the resting potential and tone of rat pulmonary artery smooth muscle. Br J Pharmacol 124: 1335–7.PubMedCrossRefGoogle Scholar