Regulation of K+ currents by CO in carotid body type I cells and pulmonary artery smooth muscle cells.

Abstract

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).