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Am J Physiol Lung Cell Mol Physiol 275: L336-L347, 1998;
1040-0605/98 $5.00
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Vol. 275, Issue 2, L336-L347, August 1998

Delayed rectifier K+ current of dog bronchial myocytes: effect of pollen sensitization and PKC activation

Gareth J. Waldron1, Stefan B. Sigurdsson2, Ernesto A. Aiello3, Andrew J. Halayko4, Newman L. Stephens4, and William C. Cole1

1 Smooth Muscle Research Group, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1; 4 Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2; 2 Department of Physiology, Faculty of Medicine, University of Iceland, Reykjavik, Iceland IS-101; and 3 Centro de Investigaciones Cardiovasculares, Facultad de Medicina, Universidad Nacional de La Plata, 1900 La Plata, Argentina

The properties of delayed rectifier K+ current [IK(dr)] of canine airway smooth muscle cells isolated from small bronchi and its modulation by protein kinase C (PKC) were studied by whole cell patch clamp. IK(dr) activated positive to -40 mV, with half-maximal activation at -16 ± 1.2 mV (n = 15) and average current density of 31 ± 2.6 pA/pF (n = 15) at +30 mV. The capacitive surface area, current density, and voltage dependence of activation of IK(dr) of myocytes of ragweed pollen-sensitized dogs were not different from age-matched control dogs. However, the sensitization reduced the availability of IK(dr) between -40 and -20 mV due to a hyperpolarizing shift in the voltage dependence of steady-state inactivation (-29.9 ± 1.2 in sensitized versus -26.0 ± 0.7 mV in control dogs, n = 9 and 11, respectively; P < 0.05). PKC activation with diacylglycerol analog or phorbol ester depressed IK(dr) amplitude, whereas an inactive diacylglycerol analog had no effect. The hyperpolarizing shift in voltage dependence of inactivation and/or modulation of IK(dr) by PKC may be two mechanisms that contribute to the enhanced reactivity of bronchial tissues from ragweed pollen-sensitized dogs.

airway smooth muscle; asthma; ragweed pollen sensitization; voltage-gated potassium channel; protein kinase C


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