title: The properties of the inward rectifier potassium currents in rabbit coronary arterial smooth muscle cells.
abstract: In freshly-isolated, single, smooth muscle cells of rabbit coronary arteries, an inward rectifier K+ current [IK(IR)] was identified using the whole-cell voltage-clamp technique. The current/voltage (I/V) relationship of IK(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 IK(IR), suggesting that the strong inward rectification of IK(IR) is partly due to the inhibitory effects of internal Mg2+. IK(IR) was unaffected by tetraethylammonium (1 mM), 4-aminopyridine (1 mM), or glibenclamide (1 microM), but was inhibited by extracellular Ba2+ with a concentration of 0.87 microM eliciting half-maximal inhibition at -120 mV. IK(IR) induced in rabbit coronary smooth muscle cells declined during very negative hyperpolarizing steps, due largely to a block by external Na+. IK(IR) was inhibited by alpha1-adrenergic stimuli. Methoxamine, an alpha1-adrenergic agonist, concentration dependently inhibited IK(IR) in the presence of the beta-adrenergic antagonist propranolol. The methoxamine concentration required for half-maximal inhibition was 205 microM. 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.
authors.affiliation: Cardiovascular Division, The Lankenau Hospital and Medical Research Center, Wynnewood, PA 19096, USA. xxujwang@aol.com
authors.forename: X
authors.initials: X
authors.lastname: Xu
authors.forename: S J
authors.initials: SJ
authors.lastname: Rials
authors.forename: Y
authors.initials: Y
authors.lastname: Wu
authors.forename: R A
authors.initials: RA
authors.lastname: Marinchak
authors.forename: P R
authors.initials: PR
authors.lastname: Kowey
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D003331:Coronary Vessels / Q000502:physiology*; D004594:Electrophysiology; D066298:In Vitro Techniques; D008274:Magnesium / Q000378:metabolism; D008297:Male; D008729:Methoxamine / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying; D011817:Rabbits; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism
chemical_list: D000316:Adrenergic alpha-Agonists; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D018340:Receptors, Adrenergic, alpha-1; D008729:Methoxamine; D008274:Magnesium; D009638:Norepinephrine