Heterogeneity of the response of venous smooth muscle to arterial endothelium-derived relaxing factor (EDRF) in respect of the role of nitric oxide

Vedernikov, Yuri P.; Gräser, T; Tiedt, N; Vikhert, A. M.

doi:10.1007/bf01907265

Cited by 11 publications

(9 citation statements)

References 10 publications

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“…Results of animal studies have suggested that NO activity is heterogenous between different venous preparations. 6,7 For example, Vedernikov et al 6 demonstrated marked endothelium-dependent relaxation in jugular, femoral, and mesenteric veins but found this was absent in the saphenous, portal, and inferior caval veins, despite preservation of endotheliumindependent relaxation in response to sodium nitroprusside.…”

Section: Role Of No In the Regulation Of Vascular Tonementioning

confidence: 99%

“…This is consistent with the findings of animal studies that demonstrated heterogeneity between different venous preparations. 6,7 It is the veins of the capacitance bed that predominantly determine overall venous tone. Therefore, our finding of both stimulated and basal NO activity in capacitance veins provides compelling new evidence that NO contributes to the regulation of venous tone and to resting venous tone in human health.…”

Section: Validation Of Techniquementioning

confidence: 99%

“…Animal studies in vivo and in vitro have shown marked heterogeneity in stimulated NO activity between different venous preparations. 6,7 Evidence of NO activity in humans has been limited to work in conduit veins (superficial hand veins and saphenous vein grafts). 8 -11 These studies have suggested that although NO activity can be stimulated by endotheliumdependent agonists, basal NO activity is absent, and therefore NO does not contribute to resting venous tone.…”

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confidence: 99%

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Endothelium-Derived Nitric Oxide Contributes to the Regulation of Venous Tone in Humans

et al. 2000

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Background-Although nitric oxide (NO) is known to play an important part in the regulation of arterial tone, little is known about its role in veins. The aim of this study was to investigate the role of basal and stimulated NO activity in the regulation of tone of the human venous capacitance bed. Methods and Results-We measured venous tone using radionuclide forearm venous plethysmography in 24 healthy subjects with no cardiovascular risk factors. In 13 subjects, basal NO activity was assessed by measuring the effects on venous tone of an intra-arterial infusion of the NO synthase inhibitor N-monomethyl-L-arginine (L-NMMA). In the remaining 11 subjects, stimulated NO activity was evaluated by measuring the effects of an intra-arterial infusion of incremental doses of carbachol, followed in a subgroup by coinfusion with L-NMMA. Infusion of carbachol caused dose-dependent venodilation, with a maximal reduction in forearm venous tone of 40.1Ϯ12.5% (PϽ0.0001). Carbachol-induced venodilation was inhibited by L-NMMA (48.9Ϯ6.2% reversal of maximal venodilation, PϽ0.01).Infusion of L-NMMA alone caused venoconstriction (9.1Ϯ6.4% increase in venous tone, Pϭ0.002). Conclusions-Human forearm capacitance veins exhibit both stimulated and basal NO activity, which indicates that NO contributes not only to the regulation of venous tone but also to resting venous tone in healthy human subjects.

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Section: Role Of No In the Regulation Of Vascular Tonementioning

confidence: 99%

Section: Validation Of Techniquementioning

confidence: 99%

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confidence: 99%

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Endothelium-Derived Nitric Oxide Contributes to the Regulation of Venous Tone in Humans

et al. 2000

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“…Several studies have suggested that NO activity varies between different venous preparations. Vedernikov et al (38) demonstrated marked endothelium-dependent relaxation in jugular, femoral, and mesenteric veins. However, such activity was not observed in the saphenous, portal, or inferior cava veins, despite preservation of endothelium-independent relaxation in response to SNP.…”

Section: Veins and Vascular Tone Control: Role Of Nomentioning

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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“…19 In addition, neither the spectrophotometric method nor the chemiluminescence method (using an acidic reducing reflux chamber) for detection of NO can distinguish it from nitrite or labile nitroso species; although the former method actually determines the concentration of NO2 derived from oxidation of NO, use of a reducing acidic refluxing chamber with the chemiluminescence method results in reduction of NO2 and nitroso compounds to NO and elimination of the high specificity for NO. Thus, neither method can determine whether the initial EDRF was NO2 or a labile nitroso substance converted to NO or whether EDRF itself was free NO.…”

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confidence: 99%

Endothelium-derived relaxing factor released from canine femoral artery by acetylcholine cannot be identified as free nitric oxide by electron paramagnetic resonance spectroscopy.

Greenberg¹,

Wilcox²,

Rubanyi³

1990

Circulation Research

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Recent studies using chemiluminescence and spectrophotometry have shown that cultured and native endothelial cells release nitric oxide (NO). Pharmacological and biochemical evidence argue for and against the proposal that endothelium-derived relaxing factor (EDRF) is identical with free NO. In an attempt to identify EDRF as free NO, a bioassay technique was combined with an NO trap (hemoglobin bound to agarose; Ag-Hb), and electron paramagnetic resonance (EPR) spectroscopy was used to detect the resultant nitrosylhemoglobin (NO-Hb). Canine femoral arteries with or without endothelium were perfused with physiological saline solution containing superoxide dismutase and ibuprofen and were stimulated with acetylcholine. The relaxing activity of the effluent was monitored in canine coronary artery rings without endothelium (bioassay tissue) half-maximally contracted with U46619. Acetylcholine stimulated the release of EDRF from intact femoral arteries (but not from segments without endothelium), which relaxed the bioassay tissue by 63+±5%. NO (-1 and -10 nM) infused directly over the bioassay tissue produced 34±8% and 96±3% relaxation, respectively (ED%, --2 nM). Effluents were collected under vacuum in the absence of oxygen through a column containing Ag-Hb, and the samples were assayed for NO-Hb by EPR. Samples containing NO produced the triplet EPR signal characteristic of NO-Hb, but the effluent containing EDRF did not. Infusion of NO through the donor tissue in the presence of acetylcholine gave an EPR signal similar to that observed when NO had no contact with the tissue. Nitrite anion (up to 2.7X 102 M) produced no detectable NO-Hb in analogous experiments. Thus, EDRF released from the native endothelium of canine femoral artery cannot be identified as free NO. The present findings support a concept that EDRF may be a labile precursor of NO. (Circulation Research 1990;67:1446-1452 E ndothelium-derived relaxing factor (EDRF) is a potent vasodilator substance released by the endothelium.1-3 Recently, it has been proposed that EDRF may be identical with nitric oxide (NO).4-6 Both pharmacological and biochemical evidence support this proposal.4-11 NO and EDRF both are inactivated by superoxide anion and hemoglobin and are protected by superoxide dismutase.4-9 The biological half-life of EDRF and NO is similar.4-9 Finally, the release of EDRF by bradykiFrom the

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Heterogeneity of the response of venous smooth muscle to arterial endothelium-derived relaxing factor (EDRF) in respect of the role of nitric oxide

Cited by 11 publications

References 10 publications

Endothelium-Derived Nitric Oxide Contributes to the Regulation of Venous Tone in Humans

Endothelium-Derived Nitric Oxide Contributes to the Regulation of Venous Tone in Humans

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

Endothelium-derived relaxing factor released from canine femoral artery by acetylcholine cannot be identified as free nitric oxide by electron paramagnetic resonance spectroscopy.

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