The effects of protein kinase C (PKC) on the tension of normal and passively sensitized human airway smooth muscle and the activity of voltage-dependent delayed rectifier potassium channel (Kv)

The effects of protein kinase C (PKC) on the tension and the activity of voltage-dependent delayed rectifier potassium channel (K-v) were examined in normal and passively sensitized human airway smooth muscle (HASM), by measuring tones and whole-cell patch clamp techniques, and the K-v activities and membrane potential (E-m) were also detected. The results showed that phorbol 12-myristate 13-acetate (PMA), a PKC activator, caused a concentration -dependent constriction in normal HASM rings. The constriction of the passively sensitized muscle in asthma serum group was significantly higher than that of the normal group (P<0.05), and the constrictions of both groups were completely abolished by PKC inhibitor Ro31-8220 and calcium channel inhibitor nifedipine. K-v activities of HASM cells were significantly inhibited by PMA, and the E-m became more positive, as compared with the DMSO (a PMA menstruum) -treated group (P<0.01). This effect could be blocked by Ro31-8220 (P<0.01). It was concluded that activation of PKC could increase the tones of HASM, which might be related to the reduced K-v activity. In passively sensitized HASM rings, this effect was more notable.