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

Schubert, Rudolf; Krien, Ulrike; Wulfsen, Iris; Schiemann, Dorrit; Lehmann, Gernot; Ulfig, Norbert; Veh, Rüdiger W.; Schwarz, Jürgen R.; Gago, Hristo

doi:10.1161/01.hyp.0000121882.42731.6b

Cited by 47 publications

(55 citation statements)

References 42 publications

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“…It suggests that the vasorelaxation effect of FLNT is mediated by NO. This finding is in agreement with previous reports showing that the vasorelaxation induced by nitrate involves NO production (25,36). In contrast, we found that nicorandil still retained most of its ability to cause relaxation of the rat aorta artery in the presence of hydroxocobalamin, which suggests that NO is not a primary factor for the nicorandil relaxation in rat aorta artery.…”

Section: Discussionsupporting

confidence: 93%

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Involvement of Guanylate Cyclase and K+ Channels in Relaxation Evoked by Ferulate Nitrate in Rat Aorta Artery

Wang¹,

Xu²,

Wang³

et al. 2012

J Pharmacol Sci

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Abstract. Vasorelaxant properties of N-2-(ferulamidoethyl)-nitrate (ferulate nitrate, FLNT), a newly synthesized nitrate, were compared with those of isosorbide dinitrate, nicorandil, nitroglycerin, and 8-bromoguanosine 3,5-cyclic monophosphate (8-Br-cGMP) in rat aorta pre-contracted by phenylephrine. FLNT produced vasorelaxation in a concentration-dependent manner (0.1 -100 μM). The degree of relaxation induced by FLNT was similar to that induced by isosorbide dinitrate. In addition, removal of endothelium did not affect the relaxant effect of FLNT. FLNT caused a rightward shift of the cumulative concentration-response curves of phenylephrine and reduced the maximal efficacy of contraction. 1H-[1,2,4]Oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ, 10 μM) and K + -channel blockers charybdotoxin (CHT, 0.1 μM) and BaCl 2 (1 μM) reduced the relaxant effect of FLNT in the endothelium-denuded arteries, whereas glibenclamide (1 μM) and 4-aminopyridine (1 mM) failed to influence FLNT-induced vasorelaxation. Furthermore, in the presence of ODQ, both CHT (0.1 μM) and BaCl 2 (1 μM) still significantly reduced the relaxation evoked by FLNT. Pretreatment of vessels with hydroxocobalamin, a nitric oxide scavenger, abolished the FLNT effect. These findings demonstrate that FLNT induces relaxation of the rat aorta rings endothelium-independently. Furthermore, we demonstrated that FLNT-induced vasorelaxation is related to its stimulation of soluble guanylate cyclase and activation of K + channels.

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Section: Discussionsupporting

confidence: 93%

“…Previous studies showed that NO donor or nitrate activated K Ca channels directly (36) or through increasing the activity of cGMP-dependent protein kinase (3,37). Another study showed that a NO donor could activate K IR by increasing the K IR current (25).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Guanylate Cyclase and K+ Channels in Relaxation Evoked by Ferulate Nitrate in Rat Aorta Artery

Wang¹,

Xu²,

Wang³

et al. 2012

J Pharmacol Sci

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“…Schubert et al (33) observed that the relaxation induced by SNP in rat tail small arteries was less potent in the presence of barium, a selective KIR blocker. In addition, SNP increased the amplitude of the KIR current, and this effect was almost abolished in the presence of barium, indicating that KIR participates in the SNP-induced relaxation.…”

Section: Hypertension and Endothelial Dysfunctionmentioning

confidence: 99%

Nitric oxide synthesis and biological functions of nitric oxide released from ruthenium compounds

Pereira

Paulo

Araújo

et al. 2011

Braz J Med Biol Res

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During three decades, an enormous number of studies have demonstrated the critical role of nitric oxide (NO) as a second messenger engaged in the activation of many systems including vascular smooth muscle relaxation. The underlying cellular mechanisms involved in vasodilatation are essentially due to soluble guanylyl-cyclase (sGC) modulation in the cytoplasm of vascular smooth cells. sGC activation culminates in cyclic GMP (cGMP) production, which in turn leads to protein kinase G (PKG) activation. NO binds to the sGC heme moiety, thereby activating this enzyme. Activation of the NO-sGC-cGMP-PKG pathway entails Ca 2+ signaling reduction and vasodilatation. Endothelium dysfunction leads to decreased production or bioavailability of endogenous NO that could contribute to vascular diseases. Nitrosyl ruthenium complexes have been studied as a new class of NO donors with potential therapeutic use in order to supply the NO deficiency. In this context, this article shall provide a brief review of the effects exerted by the NO that is enzymatically produced via endothelial NO-synthase (eNOS) activation and by the NO released from NO donor compounds in the vascular smooth muscle cells on both conduit and resistance arteries, as well as veins. In addition, the involvement of the nitrite molecule as an endogenous NO reservoir engaged in vasodilatation will be described.

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“…This indicates those kirs channels involve are in the smooth muscle relaxation via cell membrane hyperpolarization (Schubert et al, 2004). Moreover, the vasoconstrictor effect of BaCl2 due to a fact that BaCl2 interfere with BK potentiated EDHF vasodilatory mechanism.…”

Section: Discussionmentioning

confidence: 91%

The Roles of Cycloxygenase and Endothelial Derived Hyperpolarizing Factors in Bradykinin-Induced Aortic Relaxation

Omar¹,

Maulood²

2017

SJUOZ

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ABSTRACT:The present study is designed to investigate the roles of cycloxygenase (COX) and endothelial derived hyperpolarizing factors (EDHF) pathways in bradykinin (BK)-induced aortic relaxation. Here, isolated aortic rings pre-incubated with different ion channel blockers which are; inward rectifier potassium channel blocker (barium chloride; BaCl2), calcium activated Potassium (KCa+2) channel blocker (tetraethylammonium; TEA), cytochrome P450 inhibitor, clotrimazole and cycloxygenase inhibitor and indomethacin. In BaCl2, Emax tended to decrease significantly with significant change of PIC50. TEA pre-incubation markedly shifted DRC of BK to the left side and it significantly reduced PIC50. Indomethacin significantly lowered the PIC50 of BK, but it shifted the DRC of BK to the left. The results suggested that BK relaxes aortic smooth muscle particularly via the enhancement of cycloxygenase and epoxygenase enzymes as well as through opening Kir and KCa +2 channels.

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

Cited by 47 publications

References 42 publications

Involvement of Guanylate Cyclase and K+ Channels in Relaxation Evoked by Ferulate Nitrate in Rat Aorta Artery

Involvement of Guanylate Cyclase and K+ Channels in Relaxation Evoked by Ferulate Nitrate in Rat Aorta Artery

Nitric oxide synthesis and biological functions of nitric oxide released from ruthenium compounds

The Roles of Cycloxygenase and Endothelial Derived Hyperpolarizing Factors in Bradykinin-Induced Aortic Relaxation

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