Xp. Xu et al., The properties of the inward rectifier potassium currents in rabbit coronary arterial smooth muscle cells, PFLUG ARCH, 438(2), 1999, pp. 187-194
In freshly-isolated, single, smooth muscle cells of rabbit coronary arterie
s, an inward rectifier K+ current [I-K(IR)] was identified using the whole-
cell voltage-clamp technique. The current/voltage (I/V) relationship of I-K
(IR) showed strong inward rectification with a very small outward current w
hen the smooth muscle cells were dialyzed with a pipette solution containin
g Mg2+. However, dialyzing the cells with a nominally Mg2+-free pipette sol
ution revealed a significant outward current hump in the I/V relation of I-
K(IR), suggesting that the strong inward rectification of I-K(IR) is partly
due to the inhibitory effects of internal Mg2+. I-K(IR) was unaffected by
tetraethylammonium (1 mM), 4-aminopyridine (1 mM), or glibenclamide (1 mu M
), but was inhibited by extracellular Ba2+ with a concentration of 0.87 mu
M eliciting half-maximal inhibition at -120 mV. I-K(IR) induced in rabbit c
oronary smooth muscle cells declined during very negative hyperpolarizing s
teps, due largely to a block by external Na+. I-K(IR) was inhibited by al-a
drenergic stimuli. Methoxamine, an alpha(1)-adrenergic agonist, concentrati
on dependently inhibited I-K(IR) in the presence of the beta-adrenergic ant
agonist propranolol. The methoxamine concentration required for half-maxima
l inhibition was 205 mu M. We conclude that inward rectifier K+ current is
present in rabbit coronary smooth muscle cells and that it shares many prop
erties with the inward rectifier K+ current described for other cell types.