Membrane currents in canine bronchial artery and their regulation by excitatory agonists
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abstract
The bronchial vasculature plays an important role in airway physiology and pathophysiology. We investigated the ion currents in canine bronchial smooth muscle cells using patch-clamp techniques. Sustained outward K+current evoked by step depolarizations was significantly inhibited by tetraethylamonium (1 and 10 mM) or by charybdotoxin (10−6M) but was not significantly affected by 4-aminopyridine (1 or 5 mM), suggesting that it was primarily a Ca2+-activated K+current. Consistent with this, the K+current was markedly increased by raising external Ca2+to 4 mM but was decreased by nifedipine (10−6M) or by removing external Ca2+. When K+currents were blocked (by Cs+in the pipette), step depolarizations evoked transient inward currents with characteristics of L-type Ca2+current as follows: 1) activation that was voltage dependent (threshold and maximal at −50 and −10 mV, respectively); 2) inactivation that was time dependent and voltage dependent (voltage causing 50% maximal inactivation of −26 ± 22 mV); and 3) blockade by nifedipine (10−6M). The thromboxane mimetic U-46619 (10−6M) caused a marked augmentation of outward K+current (as did 10 mM caffeine) lasting only 10–20 s; this was followed by significant suppression of the K+current lasting several minutes. Phenylephrine (10−4M) also suppressed the K+current to a similar degree but did not cause the initial transient augmentation. None of these three agonists elicited inward current of any kind. We conclude that bronchial arterial smooth muscle expresses Ca2+-dependent K+channels and voltage-dependent Ca2+channels and that its excitation does not involve activation of Cl−channels.
