Nitric Oxide Release in Response to Stimulation of Nonadrenergic, Noncholinergic Nerves

Boeckxstaens, G.E.; Bult, H; Pelckmans, P.A.; Jordaens, F H; Man, Joris G. De; Ag, Herman; Maercke, Y. M. Van

doi:10.1097/00005344-199100001-00042

Cited by 10 publications

(10 citation statements)

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“…These responses are eliminated by supplementation of L-but not D-arginine (Gold et al 1989;Ress et al 1989). Introduction of NOS inhibitors (Palmer et al 1988) greatly contributed to clarifying the physiological roles of NO not only in the endothelium and vasculature but also in the immune system, the gastric mucosa (Lanas 2008), in the central (Garthwaite et al 1988) and peripheral nervous system, namely in the nonadrenergic-noncholinergic (NANC) inhibitory transmission in gut, airways, lower urinary tract, corpora cavernosa and some blood vessels (Boeckstaens et al 1990;Bauer 1993;Lefebvre 1995;Toda and Okamura 2003;Toda and Herman 2005).…”

Section: No Synthasementioning

confidence: 99%

Nitric oxide – the endothelium-derived relaxing factor and its role in endothelial functions

Bauer¹,

Sotníková²

2010

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133

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Abstract. Vascular endothelium plays a key role in the local regulation of vascular tone and vascular architecture by release of vasodilator and vasoconstrictor substances, as well as factors with pro-coagulant, anticoagulant, fibrinolytic, antibacterial properties, growth factors, chemokines, free radicals, etc. Release of endothelium-derived relaxing factors such as nitric oxide (NO), prostaglandins and endothelium-derived hyperpolarizing factor, as well as vasoconstricting factors such as endothelin, superoxide and thromboxanes play an influential role in the maintenance and regulation of vascular tone and the corresponding peripheral vascular resistance. Under physiological conditions, the release of anticoagulant and smooth muscle relaxing factors exceeds the release of other substances. The first part of this review presents the functions of the endothelium itself, the nature of the endothelium-derived relaxing factor, its production by NO synthases, mechanisms of its action via activation of soluble guanylyl cyclase and production of cyclic 3'-5'-guanosine monophosphate. The resulting biological effects include vasodilatation, regulation of vessel wall structure, increased regional blood perfusion, lowering of systemic blood pressure, antithrombosis and antiatherosclerosis effects, which counteract the vascular actions of endogenous vasoconstrictor substances. Impaired endothelial function, either as a consequence of reduced production/release or increased inactivation of endothelium-derived vasodilators, as well as interactions of NO with angiotensin, reactive oxygen species and oxidized lipoproteins, has detrimental functional consequences and is one of the most important cardiovascular risk factors. Therefore the second part of this review assesses the pathophysiologic impact of the endothelium in examples of cardiovascular pathologies, e.g. endotheliopathies caused by increased angiotensin production, lipid peroxidation, ischemia/reperfusion or diabetes.

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Section: No Synthasementioning

confidence: 99%

Nitric oxide – the endothelium-derived relaxing factor and its role in endothelial functions

Bauer¹,

Sotníková²

2010

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133

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“…The reduction in salivary flow in response to sympathetic stimulation following the administration of propranolol may also reflect the effect of the drug on the blood flow, at least in part, and likewise following administration of L-NAME, as Schachter et al (1991) (Liu, Crawley, Evans & Barnes, 1991); the present results indicate that this is likely to occur under physiological conditions. Evidence has been presented recently which strongly suggests that EDRF is released from certain populations of nerve terminals both centrally (Garthwaite, Charles & Chess-Williams, 1988) and peripherally (Gillespie, Liu & Martin, 1989;Boeckxstaens, Bult, Pelckmans, Jordaens, De Man, Herman & Van Maercke, 1991;Hollywood, Thornbury & McHale, 1992). However, this is unlikely to be the case in the sympathetic nerves of the submandibular glands in the cat, since the residual vasodilator response to stimulation of the sympathetic innervation following treatment with propranolol was abolished by dihydroergotamine (Bloom et al 1987).…”

Section: A V Edwards and J R Garrettmentioning

confidence: 99%

Endothelium‐derived vasodilator responses to sympathetic stimulation of the submandibular gland in the cat.

Edwards

Garrett

1992

The Journal of Physiology

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SUMMARY1. The extent to which vasodilator responses to electrical stimulation of the sympathetic innervation, in the submandibular gland of the cat, depend upon release of endothelium-derived relaxing factor (EDRF) within the gland has been investigated in anaesthetized cats given N-nitro-L-arginine methyl ester (L-NAME) which specifically blocks the synthesis of EDRF from arginine.2. Close intra-arterial infusions of L-NAME ( > 100 mg kg-') produced a steady and significant rise in mean aortic pressure together with a steady increase in basal submandibular vascular resistance over the next 20-30 min. It also reduced, but failed to abolish, the vasodilatation which occurs during intermittent stimulation of the sympathetic innervation (20 Hz for 1 s at 10 s intervals) together with the afterdilatation which occurs immediately after a period of continuous stimulation of these nerve fibres (2 Hz).3. In cats pretreated with the fl-blocker propranolol ( > l 0 mg kg-') both vasodilator responses were reduced, but persisted until L-NAME was administered, whereupon both were abolished.4. It is concluded that release of EDRF within the submandibular gland of the cat contributes to the basal tone of the vasculature and is responsible for the aadrenergic vasodilator responses to stimulation of the sympathetic innervation, but not for the fl-adrenergic vasodilator responses.

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“…First ATP and then VIP, were regarded as putative neurotransmitters in the gut (Burnstock et al, 1978;Manzini et al, 1986;Grider & Makhlouf, 1988). More recently, nitric oxide (NO) has been viewed as the main NANC inhibitory neurotransmitter in the gastrointestinal tract of many species (Boeckxstaens et al, 1991;Burleigh, 1992;Suthamnatpong et al, 1994;Serio et al, 1995;Takeuchi et al, 1996). However, it has become evident that IJPs may often show two phases, a fast and a slow hyperpolarization.…”

Section: Introductionmentioning

confidence: 99%

Neural modulation of the cyclic electrical and mechanical activity in the rat colonic circular muscle: putative role of ATP and NO

Plujà

Fernández

Jiménez

1999

British J Pharmacology

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1 The rat colonic circular muscle displays cyclic episodes of myenteric potential oscillations (MPOs), each of them associated with a spontaneous contraction. Nifedipine 1 mM abolished both MPOs and their associated contractions. TTX (1 mM) increased the amplitude and frequency of spontaneous contractions. 2 Electrical ®eld stimulation (EFS) induced a non-adrenergic non-cholinergic (NANC) inhibitory junction potential (IJP), with two phases: an initial fast hyperpolarization (characterized by IJP amplitude) and a sustained hyperpolarization (characterized by IJP duration). 3 Sodium nitroprusside (10 mM) hyperpolarized and abolished spontaneous contractions even in presence of TTX or 1 mM apamin. ATP (100 mM) also hyperpolarized and abolished spontaneous contractions but its e ects were decreased by TTX and abolished by apamin. 4 Suramin (100 mM) or apamin reduced the amplitude of the IJPs, but did not a ect their duration. Incubation with L-NOARG (1 mM) reduced the duration but not the amplitude of the IJPs. In presence of L-NOARG plus suramin or L-NOARG plus apamin, both duration and amplitude of the IJPs were reduced but a residual IJP could still be recorded. 5 We conclude that the mechanical and electrical cyclic activity of the rat colonic circular muscle is modulated but not originated by the enteric nervous system and involves L-type calcium channel activity. EFS induces release of NANC inhibitory neurotransmitters which hyperpolarize and relax smooth muscle cells. Both ATP and NO are involved in IJP generation: ATP is responsible for the ®rst phase of the IJPs involving activation of apamin-sensitive potassium channels, whereas NO initiates the second phase which is independent of the activation of such channels.

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Nitric Oxide Release in Response to Stimulation of Nonadrenergic, Noncholinergic Nerves

Cited by 10 publications

References 0 publications

Nitric oxide – the endothelium-derived relaxing factor and its role in endothelial functions

Nitric oxide – the endothelium-derived relaxing factor and its role in endothelial functions

Endothelium‐derived vasodilator responses to sympathetic stimulation of the submandibular gland in the cat.

Neural modulation of the cyclic electrical and mechanical activity in the rat colonic circular muscle: putative role of ATP and NO

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