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Voltage-dependent blockade of delayed rectifier K+ current by nitroprusside and ferricyanide

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Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology Aims and scope

Abstract

NO donor nitroprusside (NP) is a biologically active drug with hypotensive and neurotropic properties. Its effects are due to NO as well as to other derivates, specifically ferricyanide (FC) and ferrocyanide (F(2+)C) ions. In the present work we studied effects of NP, FC, and F(2+)C on delayed rectifier K+ current. The experiments were conducted on isolated neurons of land snail Helix using two-microelectrode voltageclamp technique. Delayed rectifier K+ current often displayed abnormal rectification. NP (1 mM) caused voltage-dependent reduction of K+ current, which looked like enhancement of the abnormal rectification. FC (1 mM)—but not F(2+)C—acted likewise; the effects of NP and FC were not additive. Dibutiryl cGMP (dbcGMP) had an opposite effect, weakening abnormal rectification of the K+ current. Protein kinase inhibitor H-8 (10 μM) caused voltage-dependent reduction of the K+ current, as NP and FC did. The effects of H-8 and NP and effects of H-8 and FC were not additive. The results suggest that: (i) NP effects on delayed rectifier K+ current are mediated by FC and (ii) the effects of these drugs involve phosphorylation processes.

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Correspondence to E. I. Solntseva.

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Original Russian Text © E.I. Solntseva, J.V. Bukanova, V.G. Skrebitsky, 2009, published in Biologicheskie Membrany, 2009, Vol. 26, No. 6, pp. 486492–123123123.

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Solntseva, E.I., Bukanova, J.V. & Skrebitsky, V.G. Voltage-dependent blockade of delayed rectifier K+ current by nitroprusside and ferricyanide. Biochem. Moscow Suppl. Ser. A 3, 431–437 (2009). https://doi.org/10.1134/S1990747809040102

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  • DOI: https://doi.org/10.1134/S1990747809040102

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