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

R. Schubert, U. Krien, I. Wulfsen, D. Schiemann, G. Lehmann, N. Ulfig, R. W. Veh, J. R. Schwarz, H. Gago
2004 Hypertension  
The role of vascular smooth muscle inward rectifier K ϩ (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 2.6ϫ10 Ϫ8 mol/L. Endothelium removal did not attenuate this effect. Vessel pretreatment with hydroxocobalamin, a nitric oxide (NO) scavenger, but not with rhodanese and sodium
more » ... and sodium thiosulfate, inactivators of cyanide (CN), abolished the SNP effect. Vessel pretreatment with 10 Ϫ5 mol/L Ba 2ϩ , a specific blocker of K IR channels at micromolar concentrations, reduced the SNP effect. Low concentrations of K ϩ dilated the vessels; this effect was attenuated largely after pretreatment with 3ϫ10 Ϫ5 mol/L Ba 2ϩ . In freshly isolated smooth muscle cells, a barium-sensitive current was observed at potentials negative to the potassium equilibrium potential. Application of 10 Ϫ4 mol/L SNP increased the barium-sensitive current 1.79Ϯ0.23fold at Ϫ100 mV and hyperpolarized the membrane potential by 8.6Ϯ0.5 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. (Hypertension. 2004;43:891-896.)
doi:10.1161/01.hyp.0000121882.42731.6b pmid:14993195 fatcat:wccjbhsotbejbcxv7zqcbmykzm