Vasodilatation in the dental pulp produced by electrical stimulation of the inferior alveolar nerve in the cat

Gazelius, Bertil; Olgart, Leif

doi:10.1111/j.1748-1716.1980.tb06516.x

Cited by 74 publications

(28 citation statements)

References 29 publications

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“…There is now consistent evidence that release of a neurotransmitter from sensory nerves can be responsible for wheal and distant flare formation following trauma (Jancso et al, 1968;Lembeck & Holzer, 1979;Gazelius & Olgart, 1980;Anand et al, 1983;Lundberg et al, 1983;Kenins et al, 1984). This study suggests wheal formation following trauma may be due to release ofa tachykinin, either SP, NKA or NKB rather than release of CGRP which does not lead to wheal formation.…”

Section: Discussionmentioning

confidence: 59%

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Sensory neuropeptide effects in human skin

Fuller

Conradson

Dixon

et al. 1987

British J Pharmacology

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1Neuropeptides released from sensory nerves may account for cutaneous flare and wheal following local trauma. In 28 normal subjects we have studied the effects of four sensory neuropeptides given by intradermal injection on the forearm or back. 2 All peptides caused a flare distant from the site of injection, presumably due to an axon reflex. Substance P (SP) was the most potent (geometric mean dose causing 50% ofmaximum flare, 4.2 pmol). Neurokinin A (NKA) was the next most potent with neurokinin B (NKB) and calcitonin gene-related peptide (CGRP) the least. The distant flare response to SP, NKA and NKB was maximal at 5 min and disappeared within 2 h. 3 CGRP caused a local erythema over the site of injection at doses above 0.5 pmol which at higher doses lasted for up to 12 h. 4 SP, NKA and NKB caused wheals at doses above 5 pmol with SP and NKB being the most potent. CGRP (up to 250 pmol) did not consistently cause wheal formation. There was no significant effect of coinjection ofCGRP upon the response to SP although there was a tendency for an enhancement ofthe wheal response. 5 The H,-histamine antagonist terfenadine (60mg orally) significantly inhibited the wheal and distant flare response to histamine (5 nmol) and NKA, but not that caused by NKB. The distant flare of CGRP was also reduced but the local erythema was unaltered. 6 Aspirin (600 mg orally) significantly inhibited the distant flare response to SP, NKA and CGRP, but not that caused by NKB or histamine; the local erythema induced by CGRP was unaffected by aspirin. Aspirin also inhibited the wheal formed by NKA but not the wheal induced by the other substances. 7 These results suggest that tachykinins cause a distant flare response partially via the release of histamine and cyclo-oxygenase products, but cause a wheal by a direct effect on the skin microvasculature. The order of potency SP > NKB > NKA suggests that an SPp or NK, receptor is involved in the wheal response. CGRP by contrast has a direct vasodilator effect which is very prolonged.

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Section: Discussionmentioning

confidence: 59%

“…The widespread flare and part of the wheal response are dependent on intact sensory nerves (Jancso et al, 1968) and probably release of sensory neurotransmitters by an axon reflex (Chahl, 1979;Lembeck & Holzer, 1979;Gazelius & Olgart, 1980;Brodin et al, 1981;Anand et al, 1983; 'Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Sensory neuropeptide effects in human skin

Fuller

Conradson

Dixon

et al. 1987

British J Pharmacology

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“…There is evidence that SP may be involved in the vascular effects caused by antidromic activation of sensory afferents (Lembeck & Holzer, 1979); these effects include vasodilatation (Gazelius & Olgart, 1980) and an inflammatory response, e.g. in the eye with increased intraocular pressure and breakdown of the blood-aqueous barrier (Bill et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

Characterization of tachykinin receptors in isolated basilar arteries of guinea‐pig

Edvinsson

Jansen

1987

British J Pharmacology

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1 In circular lengths cut from the basilar artery of guinea-pig (0.2-0.3 mm o.d.) relaxations induced by substance P and neurokinin A were highly susceptible to mechanical damage of the endothelium by rubbing. The precontraction induced by prostaglandin F2, but not that of 124 mm potassium was reduced considerably by the rubbing procedure. 2 Concentration-dependent relaxations were evoked by tachykinin agonists in the following order of potency: substance P = physalaemin> neurokinin A > eledoisin. Physalaemin was, however, a partial agonist, giving only half the maximum relaxation as compared to the other tachykinins. 4 The results suggest the presence of tachykinin receptors of the 'SP-P' type in guinea-pig basilar arteries which, for induction of relaxation, involves the release of an endothelium-derived relaxing factor.

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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%

“…The involvement of a p-adrenoceptor-mediated vasodilator component in the sympathetic control of pulpal blood flow has been a matter of great controversy (Tonder, 1976;Heyeraas Tonder and Naess, 1978;Gazelius and Olgart, 1980;Kim et al, 1980). Although local application of p-adrenoceptor agonists on the pulp causes vasodilation, thereby implying the presence of these receptors in the pulp (Okabe et al, 1989;Liu et al, 1990), there is little evidence that they have any significance in neural control.…”

Section: Sympathetic Systemmentioning

confidence: 99%

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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Vasodilatation in the dental pulp produced by electrical stimulation of the inferior alveolar nerve in the cat

Cited by 74 publications

References 29 publications

Sensory neuropeptide effects in human skin

Sensory neuropeptide effects in human skin

Characterization of tachykinin receptors in isolated basilar arteries of guinea‐pig

Neural Control of Pulpal Blood Flow

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