K+ channels and their effects on membrane potential in rat bronchial smooth muscle cells.

In order to investigate the K+ channels and their effects on resting membrane potential (Em) and excitability in rat bronchial smooth muscle cells (BSMCs), the components of outward K+ channel currents and the effects of K+ channels on Em and tension in rat bronchial smooth muscle were observed by using standard whole-cell recording of patch clamp and isometric tension recording techniques. The results showed that under resting conditions, total outward K+ channel currents in freshly isolated BSMCs were unaffected by ATP-sensitive K+ channel blocker. There were two types of K+ currents: voltage-dependent delayed rectifier K+ channel (Kv) and large conductance calcium-activated K+ channel (BKCa) currents. 1 mmol/L 4-aminopyridine (4-AP, an inhibitor of Kv) caused a significant depolarization (from -8.7 +/- 5.9 mV to -25.4 +/- 3.1 mV, n = 18, P < 0.001). In contrast, 1 mmol/L tetraethylammonium (TEA, an inhibitor of BKca) had no significant effect on Em (from -37.6 +/- 4.8 mV to -36.8 +/- 4.1 mV, n = 12, P > 0.05). 4-AP caused a concentration-dependent contraction in resting bronchial strips. TEA had no effect on resting tension, but application of 5 mmol/L TEA resulted in a left shift with bigger pD2 (the negative logarithm of the drug concentration causing 50% of maximal effect) (from 6.27 +/- 0.38 to 6.89 +/- 0.54, n = 10, P < 0.05) in the concentration-effect curve of endothine-1, and a right shift with smaller pD2 (from 8.10 +/- 0.23 to 7.69 +/- 0.08, n = 10, P < 0.05) in the concentration-effect curve of isoprenaline. It was suggested that in rat BSMCs there may be two types of K+ channels, Kv and BKca, which serve distinct roles. Kv participates in the control of resting Em and tension. BKca is involved in the regulation of relaxation or contraction associated with excitation.