Am. Evans et al., PROPERTIES OF A NOVEL K-ARTERY SMOOTH-MUSCLE CELLS( CURRENT THAT IS ACTIVE AT RESTING POTENTIAL IN RABBIT PULMONARY), Journal of physiology, 496(2), 1996, pp. 407-420
1. An outward current (I-K(N)) was identified in rabbit pulmonary arte
ry myocytes, which persisted after Ca2+-activated and ATP-sensitive K currents were blocked by TEA (10 mM) and glibenclamide (10 mu M), res
pectively, and after A-like (I-K(A)) and delayed rectifier (I-K(V)) K currents were inactivated by clamping the cell at 0 mV for >10 min. I
t was found in smooth muscle cells at all levels of the pulmonary arte
rial tree. 2. The relationship between the reversal potential of I-K(N
) and the extracellular K+ concentration ([K+](o)) was close to that e
xpected for a K+-selective channel. Deviation from Nernstian behaviour
at low [K+](o) could be accounted for by the presence of an accompany
ing leakage current. 3. I-K(N) is voltage gated. It has a low threshol
d for activation, between -80 and -65 mV, and activates slowly without
delay. Activation follows an exponential time course with a time cons
tant of 1.6 s at -60 mV. Deactivation is an order of magnitude faster-
than activation, with a time constant of 107 ms at -60 mV. 4. I-K(N) s
howed a similar sensitivity to 4-aminopyridine as I-K(A) and I-K(V), w
ith 49% inhibition at 10 mM. The current was not blocked by 10 mu M qu
inine, which did inhibit I-K(A) and I-K(V), by 51 and 47%, respectivel
y. 5. Activation of I-K(N) was detected at potentials close to the res
ting membrane potential of pulmonary artery smooth muscle cells, under
physiological conditions. Thus it is likely to contribute to the rest
ing membrane potential of these cells.