Nitric Oxide Donor Sodium Nitroprusside Dilates Rat Small Arteries by Activation of Inward Rectifier Potassium Channels

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Abstract
The role of vascular smooth muscle inward rectifier K + (K IR ) channels in the mechanisms underlying vasodilation is still unclear. The hypothesis that K IR channels are involved in sodium nitroprusside (SNP)-induced dilation of rat-tail small arteries was tested. SNP relaxed tail small arteries with an EC 50 of 2.6×10 −8 mol/L. Endothelium removal did not attenuate this effect. Vessel pretreatment with hydroxocobalamin, a nitric oxide (NO) scavenger, but not with rhodanese and sodium thiosulfate, inactivators of cyanide (CN), abolished the SNP effect. Vessel pretreatment with 10 −5 mol/L Ba 2+ , a specific blocker of K IR channels at micromolar concentrations, reduced the SNP effect. Low concentrations of K + dilated the vessels; this effect was attenuated largely after pretreatment with 3×10 −5 mol/L Ba 2+ . In freshly isolated smooth muscle cells, a barium-sensitive current was observed at potentials negative to the potassium equilibrium potential. Application of 10 −4 mol/L SNP increased the barium-sensitive current 1.79±0.23-fold at −100 mV and hyperpolarized the membrane potential by 8.6±0.5 mV. In tissue from freshly dissected vessels, transcripts for K IR 2.1 and 2.2, but not for K IR 2.3 and 2.4, were found. However, only K IR 2.1 antibodies immunostained the tunica media of the vessel. These data suggest that vascular smooth muscle K IR 2.1 channels are involved in the SNP-induced dilation of rat-tail small arteries.