The autonomic innervation of the nasal blood vessels of the cat

Eccles, Ronald; Wilson, H.

doi:10.1113/jphysiol.1974.sp010542

Cited by 91 publications

(50 citation statements)

References 7 publications

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“…One was atropine-sensitive and accounted for about 50% ofthe amplitude of the dilatation but the other was unaffected by concentrations ofatropine ofup to 10-6 M. This type of mixed dilator response is not unusual; it has been noted in a number of different tissues including the cat salivary gland (Lundberg, 1981), nasal mucosa (Eccles & Wilson, 1974), tongue (Bevan et al, 1982;Lundberg et al, 1982) and the dog hind limb (Brody & Shaffer, 1970).…”

Section: Discussionmentioning

confidence: 99%

“…For instance, stimulation of the sympathetic neural outflow to skeletal muscles of the cat and dog can evoke an atropine-sensitive vasodilatation, which is particularly evident when constrictor responses have been inhibited or in the presence of physostigmine (Builbring & Burn, 1935 parasympathetic in origin have been noted in the cat cephalic circulation, specifically in blood vessels supplying the salivary glands (Lundberg, 1981), nasal mucosa (Eccles & Wilson, 1974), brain (Chorobski & Penfield, 1932, Bevan et al, 1982, and tongue (Lundberg et al, 1982;Bevan et al, 1982). Such vascular responses have also been demonstrated in the guineapig uterine artery (Bell, 1968).…”

Section: Introductionmentioning

confidence: 99%

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Electrophysiological analysis of neurogenic vasodilatation in the isolated lingual artery of the rabbit

Brayden

Large

1986

British J Pharmacology

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With parameters similar to those used in the mechanical studies, periarterial stimulation in the presence of guanethidine evoked membrane hyperpolarizations which achieved amplitudes of up to 11 mV. The ionophoretic application of acetylcholine (ACh) produced hyperpolarization. 4 The inhibitory junction potentials (ij.ps) but not the ionophoretic-induced responses were blocked by TTX. The nerve-evoked and the ACh-induced hyperpolarizations were potentiated by physostigmine (5 x 10-7 M) and totally blocked by atropine (10-7 M).5 Ij.ps and hyperpolarization to ionophoresis of ACh were recorded from arteries in which the endothelium had been removed by mechanical rubbing. Mechanical relaxation to field stimulation and ACh was observed in preparations without endothelium. 6 These data suggest that the cholinergic component of the neurogenic vasodilatation in the rabbit lingual artery is accompanied by hyperpolarization. The non-cholinergic component does not appear to possess an electrophysiological correlate. In addition, it seems that the action of nerve-released ACh is mediated by muscarinic receptors which are situated directly on the vascular smooth muscle cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Electrophysiological analysis of neurogenic vasodilatation in the isolated lingual artery of the rabbit

Brayden

Large

1986

British J Pharmacology

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“…Electrical stimulation of the cervical sympathetic nerve causes a pronounced nasal vasoconstriction and a decrease in nasal airway resistance [32,[40][41][42][43][44][45][46]. The spontaneous reciprocal changes in nasal airway resistance, which constitute the nasal cycle, have been reported to be abolished after section of the cervical sympathetic nerve or local anaesthesia of the stellate ganglion [32,47,48].…”

Section: Autonomic Control Of Nasal Venous Sinusoidsmentioning

confidence: 99%

A role for the nasal cycle in respiratory defence

Eccles¹

1996

Eur Respir J

106

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This review describes the phenomenon of the nasal cycle, which consists of periodic congestion and decongestion of the nasal venous sinusoids.The hypothesis is put forward that the nasal venous sinusoids participate in respiratory defence by generation of plasma exudate. This hypothesis is based on recent studies, which have shown that the nasal venous sinusoids have a fenestrated endothelium and that the nasal cycle is increased during periods of nasal infection; and also on a series of older observations in the literature, which link the generation of nasal fluid to the decongestion of nasal venous sinusoids.It is proposed that the periodic congestion and decongestion of nasal venous sinusoids may provide a pump mechanism for the generation of plasma exudate, and that this mechanism is an important component of respiratory defence.

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“…The measurements of nasal blood flow and nasal mucosa volume in the cat and the dog have been previously performed using indirect methods (Anggard & Densert, 1974;Eccles & Wilson, 1974;Berridge & Roach, 1986). The procedure used in the present study was originally developed in the pig (Lacroix et al 1988) and allowed simultaneous direct recordings of changes in arterial blood flow and volume of the nasal mucosa.…”

Section: Resultsmentioning

confidence: 99%

The role of ATP in non‐adrenergic sympathetic vascular control of the nasal mucosa in anaesthetized cats and dogs.

Lacroix¹,

Ulman²,

Potter³

1994

The Journal of Physiology

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1. In anaesthetized cats and dogs, local intra-arterial injection of noradrenaline and a, fl-methylene adenosine 5'-triphosphate (mATP) reduced both nasal arterial blood flow and nasal mucosal volume (a measure of capacitance vessel function). The responses to mATP were not modified by pretreatment with the adrenoceptor antagonists phentolamine and propranolol or the purinoceptor antagonist suramin. The vascular effects of noradrenaline were not altered by suramin, but were virtually abolished by adrenoceptor antagonists. 2. After adrenoceptor blockade, frequency-dependent reductions in nasal arterial blood flow with sympathetic nerve stimulation were reduced by 25 and 39 % in cats and dogs, respectively; whereas the volume response was reduced by 56 % in cats and 54 % in dogs.The remaining non-adrenergic sympathetic nerve-evoked vascular responses were not influenced by suramin. 3. During desensitization to mATP induced by local intra-arterial infusion for 5 min, the remaining non-adrenergic nasal blood flow and volume responses to sympathetic nerve stimulation were reduced in the dog but not in the cat. 4. It is suggested that both adrenergic and non-adrenergic mechanisms are involved in the sympathetic control of the nasal mucosa vascular bed of both species. Since desensitization to mATP markedly reduces the remaining non-adrenergic nasal vasoconstriction evoked by sympathetic nerve stimulation in the dog, ATP is a possible sympathetic mediator in the nasal vascular bed in this species.

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The autonomic innervation of the nasal blood vessels of the cat

Cited by 91 publications

References 7 publications

Electrophysiological analysis of neurogenic vasodilatation in the isolated lingual artery of the rabbit

Electrophysiological analysis of neurogenic vasodilatation in the isolated lingual artery of the rabbit

A role for the nasal cycle in respiratory defence

The role of ATP in non‐adrenergic sympathetic vascular control of the nasal mucosa in anaesthetized cats and dogs.

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