Differential effects of nitric oxide synthesis inhibition on basal blood flow and antidromic vasodilation in rat oral tissues

Kerezoudis, Nikolaos P.; Olgart, Leif; Edwall, L.

doi:10.1016/0014-2999(93)90205-v

Cited by 49 publications

(43 citation statements)

References 43 publications

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“…However, this hypothesis was not supported by the inability of L-NAME to inhibit the increase of cutaneous blood flow elicited by antidromic stimulation of the saphenous nerve. NO has likewise been ruled out as a contributor to antidromic vasodilatation in the pulp and lip of the rat, which is not reduced but augmented by L-NAME (Kerezoudis et al, 1993). The chief, if not exclusive, mediator of antidromic vasodilatation evoked by saphenous nerve stimulation (Delay-Goyet et al, 1992;Escott & Brain, 1993) or local application of capsaicin (Hughes & Brain, 1991; is CGRP.…”

Section: Discussionmentioning

confidence: 99%

Cutaneous vasodilatation induced by nitric oxide‐evoked stimulation of afferent nerves in the rat

Holzer

Jocič

1994

British J Pharmacology

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1 The site of action at which nitric oxide (NO) may contribute to neurogenic vasodilatation in the hindpaw skin of urethane-anaesthetized rats was examined by the use of N0-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase. 2 Skin blood flow was measured by laser Doppler flowmetry, and neurogenic vasodilatation was evoked either by topical application of mustard oil (5%) or antidromic electrical stimulation of the saphenous nerve (antidromic vasodilatation).3 L-NAME (60 lmol kg-', i.v.) attenuated the hyperaemia evoked by mustard oil in an enantiomerspecific manner but failed to reduce antidromic vasodilatation and the vasodilatation due to i.v. injected calcitonin gene-related peptide (CGRP) and substance P (0.1-1 nmol kg-each), two proposed mediators of neurogenic vasodilatation. 4 Pretreatment of rats with capsaicin (125 mg kg', s.c. 2 weeks beforehand), to defunctionalize afferent neurones, reduced the hyperaemic response to mustard oil and prevented L-NAME from further decreasing the vasodilatation evoked by mustard oil. 5 Intraplantar infusion of sodium nitroprusside (SNP, 0.15 nmol in 1 min), a donor of NO, induced hyperaemia which was significantly diminished by the CGRP antagonist i.v.) and by capsaicin pretreatment. The ability of CGRP8-37 to inhibit the vasodilator response to SNP was lost in capsaicin-pretreated rats. 6 Taken together, these data indicate that NO does not play a vasorelaxant messenger role in neurogenic vasodilatation but can contribute to activation of, and/or transmitter release from, afferent nerve fibres in response to irritant chemicals.

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Section: Discussionmentioning

confidence: 99%

Cutaneous vasodilatation induced by nitric oxide‐evoked stimulation of afferent nerves in the rat

Holzer

Jocič

1994

British J Pharmacology

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“…Activation of sensory nerves in the pulp, either by brief antidromic electrical stimulation of the inferior alveolar nerve or by direct stimulation on the tooth crown, induces a long-lasting blood flow increase in the pulp (Heyeraas Tonder and Naess, 1978;Gazelius and Olgart, 1980;Kerezoudis et al, 1993b). The mechanism of this reaction in rat incisor pulp was recently shown to involve both SP and CGRP (Kerezoudis et al, 1994a,b).…”

Section: Non-adrenergic Non-cholinergic Vasodilator Nervesmentioning

confidence: 99%

“…Under basal blood flow conditions, NO appears to play a role in modulating the local myogenic tone of pulpal vessels (Kerezoudis et al, 1993b). Thus, a basal formation of NO appears to be maintained as a consequence of the continuous enzyme activation of the endothelium, e.g., by shear stress.…”

Section: Other Mechanisms Modulating Pulpal Blood Flowmentioning

confidence: 99%

“…Thus, a basal formation of NO appears to be maintained as a consequence of the continuous enzyme activation of the endothelium, e.g., by shear stress. Support for a role of NO in regulation of vascular tone was obtained in studies on rat incisors and cat canine teeth which showed that treatment with an inhibitor of NO-synthase caused vasoconstriction (Kerezoudis et al, 1993b;Lohinai et al, 1995). Since the vascular endothelium continously generates both a vasoconstrictor substance (ET) and a vasodilator agent (NO), there are prerequisites for modulation of pulp circulation without influence of nerves.…”

Section: Other Mechanisms Modulating Pulpal Blood Flowmentioning

confidence: 99%

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Neural Control of Pulpal Blood Flow

Olgart

1996

Critical Reviews in Oral Biology & Medicine

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Blood flow of mammalian dental pulp is under both remote and local control. There is evidence for the existence of parasympathetic nerves in the pulp, but functionally the cholinergic influence is weak, and the physiological significance of this autonomic system seems to be low. The evidence for sympathetic vasoconstrictor nerves in the pulp is robust, and there is convincing support for the contention that these nerves play a physiological role, operating via release of noradrenaline and neuropeptide Y. However, there is no significant functional evidence in support of sympathetic beta-adrenoceptor-mediated vasodilation in the pulp. The local control of blood flow involves a subset of intradental sensory nerves. By virtue of their neuropeptide content, these afferent fibers cause vasodilation and inhibit sympathetic vasoconstriction in response to painful stimulation of the tooth. Such locally governed control may serve to meet immediate demands of the pulp tissue. A locally triggered reflex activation of sympathetic nerves in the pulp may modulate this control and limit its magnitude. Thus, there are competitive interactions between local and remote vascular controls which may be put out of balance in the injured and inflamed dental pulp.

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“…However, there are some physiological data to suggest an essential role for nitric oxide in the haemodynamic regulation of rat (Kerezoudis et al 1993) and cat (Lohinai et a1. 1995) dental pulp and in rat gingiva (Fazekas et al 1994). Nitric oxide synthase-containing nerves have been identified in cat dental pulp and in cat and dog gingiva (Lohinai et al 1997).…”

mentioning

confidence: 99%

In vitro Cytotoxicity of the Nitric Oxide Donor, S‐Nitroso‐N‐acetyl‐peraciUamine, towards Cells from Human Oral Tissue

Babich

Zuckerbraun

Hirsch

et al. 1999

Pharmacology & Toxicology

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Abstract; The cytotoxicity of the nitric oxide donor, S-nitroso-N-acetyl-penicillamine (SNAP), towards cultured human cells from oral tissue was evaluated. The toxicity of SNAP to Smulow-Glickman gingival epithelial cells was correlated with the liberation of nitric oxide, as N-acetyl-D,L-penicillamine. the SNAP metabolites, N-acetyl-D,L-penicillamine disulfide and nitrite, and preincubated (denitrosylated) SNAP did not affect viability. Comparing equimolar concentrations of various nitric oxide donors, cytotoxicity appeared to be inversely related to the relative stability (i.e.. half-life) of the test compound; the sequence of cytotoxicity for a 4 hr exposure was S-nitrosoglutathione>>spermine NONOate> SNAP>DPTA NONOate>>DETA NONOate. Intracellular reduced glutathione (GSH) was lowered in S-G cells exposed to SNAP Pretreatment of the cells with the GSH depleter, 1.3-bis-(chloroethyl)-l-nitrosourea (BCNU), enhanced the toxicity of SNAP Similar findings of enhanced sensitivity to SNAP were noted with gingival fibroblasts and periodontal ligament cells pretreated with BCNU. The toxicity of SNAP towards the gingival epithelial cells was decreased by cotreatment with the antioxidants, N-acetyl-L-cysteine, L-ascorbic acid, and (+)-catechin. Cells exposed to SNAP exhibited nuclear aberrations, including multilobed nuclei and multinucleation. SNAP-induced cell death was apparently by apoptosis, as noted by fluorescence microscopy and DNA agarose gel electrophoresis.Nitric oxide is a free radical gas endogenously synthesized in many cell types from L-arginine by nitric oxide synthase. It has a diverse spectrum of physiological functions, including smooth muscle relaxation, regulation of vascular tone, neurotransmission, inhibition of intercellular platelet adhesion and aggregation, reduction of white blood cell adhesion to endothelial cells, and macrophage-induced cytotoxicity. Situations in which high and sustained amounts of nitric oxide are produced by induction of nitric oxide synthase include tumor growth, inflammation, wound healing, and sepsis, in which cytokines and bacterial endotoxins are released (Nathan 1992;Moncada & Higgs 1993).Over-production of nitric oxide may induce pathological conditions. On a cellular level, the main targets of nitric oxide are thiol groups of proteins, frequently found in cell membranes. These reduced thiols react with nitric oxide to yield S-nitrosothiols (Ignarro et al. 1981). Due to its lipophilicity or its interaction with thiols, nitric oxide can pass easily into the intracellular area and adversely affect cell metabolism. For example, exogenous nitric oxide generated from the chemical donor, S-nitroso-N-acetyl-penicillamine (SNAP), inhibited protein synthesis (Curran et al.

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Differential effects of nitric oxide synthesis inhibition on basal blood flow and antidromic vasodilation in rat oral tissues

Cited by 49 publications

References 43 publications

Cutaneous vasodilatation induced by nitric oxide‐evoked stimulation of afferent nerves in the rat

Cutaneous vasodilatation induced by nitric oxide‐evoked stimulation of afferent nerves in the rat

Neural Control of Pulpal Blood Flow

In vitro Cytotoxicity of the Nitric Oxide Donor, S‐Nitroso‐N‐acetyl‐peraciUamine, towards Cells from Human Oral Tissue

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