The properties of the inward rectifier potassium currents in rabbit coronary arterial smooth muscle cells

In freshly-isolated, single, smooth muscle cells of rabbit coronary arteries, 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 when the smooth muscle cells were dialyzed with a pipette solution containing Mg2+. However, dialyzing the cells with a nominally Mg2+-free pipette solution 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 coronary smooth muscle cells declined during very negative hyperpolarizing steps, due largely to a block by external Na+. I-K(IR) was inhibited by al-adrenergic stimuli. Methoxamine, an alpha(1)-adrenergic agonist, concentration dependently inhibited I-K(IR) in the presence of the beta-adrenergic antagonist propranolol. The methoxamine concentration required for half-maximal 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 properties with the inward rectifier K+ current described for other cell types.