Inhibition of the Pial Artery Constriction Induced by Sympathetic Stimulation by Local Microapplication of a Cholinomimetic Agent

Sercombe, Richard; Wahl, Michael

doi:10.1038/jcbfm.1982.51

Cited by 8 publications

(4 citation statements)

References 14 publications

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“…Stimu lation of the sympathetic fibers, at the level of the superior of sensory fibers to the brain vessels in rat has also been shown to cause a minor increase in CBF ipsilaterally [8], Removal of the parasympathetic or sensory nerves does not affect resting blood flow [7][8][9][10][11][12], There is evidence for a close anatomical interrelation ship among these fiber types in the pial vessels, both as identical courses along the vascular branches [13][14][15] and at the terminal level [14,16,17]. Pharmacological experi ments indicate that cholinergic receptors are located on sympathetic nerve terminals [18][19][20][21]. Some of these stud ies claim that acetylcholine blocks the release of noradren aline [18,20,21].…”

Section: Introductionmentioning

confidence: 99%

“…Pharmacological experi ments indicate that cholinergic receptors are located on sympathetic nerve terminals [18][19][20][21]. Some of these stud ies claim that acetylcholine blocks the release of noradren aline [18,20,21]. There is physiopharmacological evi dence in cat for an interaction between the sympathetic and sensory nerves in pial arterioles: the vasoconstrictor action of noradrenaline is prolonged after sectioning of the trigeminal nerve [9], which may indicate that the tri geminal cerebrovascular nerves provide a reflex mecha nism to overcome reductions in CBF.…”

Section: Introductionmentioning

confidence: 99%

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Interaction between Cerebrovascular Sympathetic, Parasympathetic and Sensory Nerves in Blood Flow Regulation

1993

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Morphological and pharmacological findings support that different cerebrovascular nerve types have close relationships in the vessel wall and that interactions may contribute to the control of vascular tone. This study in rat investigates whether interaction in blood flow regulation occurs between sympathetic, parasympathetic and sensory nerves in the cerebral vessels. Cortical blood flow (CBF) was measured with a laser-Doppler flowmeter during electrical stimulation of one of the nerves, with or without prior denervation of one or two of the other nerves. Unilateral sympathetic stimulation significantly decreased CBF ipsilaterally. The response was unaffected in magnitude and time course by parasympathetic or sensory denervation. Sensory nerve stimulation did not significantly affect CBF, even after sympathetic denervation. Parasympathetic nerve stimulation caused a marked increase in CBF, which was similar in magnitude in the presence or absence of sympathetic innervation. However, the return to the basal CBF level after parasympathetic stimulation was prolonged after sympathetic denervation. Thus, activation of the sympathetic nerves may contribute to a rapid normalization of the enhanced CBF during parasympathetic nerve stimulation, whereas the reverse phenomenon, parasympathetic normalization of the sympathetically induced CBF reduction, does not occur.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interaction between Cerebrovascular Sympathetic, Parasympathetic and Sensory Nerves in Blood Flow Regulation

1993

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“…However, as in dicated above, there appeared to be no significant uptake of 5-HT by sympathetic nerves in our experimental conditions. In addition, the presynaptic choline@ receptors on sympathetic nerve terminals inhibit norepinephrine release (3,13,31). Because norepinephrine and 5-HT are probably stored (6) and released together (23,32), cholinergic stimulation of sympathetic nerve terminals would tend to decrease 5-HT efflux rather than increase it.…”

Section: Discussionmentioning

confidence: 99%

Carbachol induces granular cell exocytosis and serotonin release in rabbit cerebral arteries

Reynier-Rebuffel

Crinon

Dimitriadou

et al. 1992

American Journal of Physiology-Regulatory, Integrative and Comp

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Previously, we reported that rabbit cerebral arteries contain mast cells that frequently establish close contacts with parasympathetic-like nerve fibers. Here we have examined the possible function of this link by comparing the effects of carbachol and compound 48/80 on mast cell morphology and on the serotonin (5-HT) and histamine content of these arteries. In vivo, 2 micrograms/min of compound 48/80 or 1 micrograms/min of carbachol was infused for 30 min into one internal carotid artery of pentobarbital anesthetized rabbits, the contralateral artery being infused with vehicle. In vitro, the action of 10(-6) M carbachol was tested on isolated middle cerebral artery trees (MCAs) in the presence or absence of 10(-7) M atropine. The effects of carbachol were also tested in vitro on sympathectomized arteries. The 5-HT and histamine contents of all MCAs were measured by radioenzymatic assay, and fragments were prepared for electron microscopy. No histamine was detectable in any artery studied. The 5-HT content of arteries from control animals and those perfused with vehicle (in vivo) or incubated in the physiological solution (in vitro) was 250-300 pmol/mg protein. Both compound 48/80 and carbachol reduced this amount by approximately 50% and induced a marked degranulation of mast cells. Both secretion and degranulation were dramatically blocked in vitro by atropine. No difference in the 5-HT content was observed between intact and sympathectomized arteries under any condition. We conclude that a large proportion of rabbit cerebrovascular 5-HT is stored in mast cells and that cholinergic nerve activation could theoretically release this pool by acting on mast cell muscarinic receptors.

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“…High concentrations (10-4-10-3 M) of nicotine have been found to dilate extraparenchymal cerebral arteries directly when applied the perivascular space (Wahl and Kuschinsky 1977a). Furthermore, nicotine acting on prejunctional receptors of postganglionic sympathetic cerebrovascular fibres may inhibit the release of norepinephrine (Edvinsson et al 1977) and thus reduce the vasoconstrictor response (Aubineau et al 1980;Sercombe and Wahl 1982). The latter appears to be specific to the cerebral circulation since in other organs the release of norepinephrine from perivascular nerves is facilitated by prejunctional nicotinic receptors but inhibited by prejunctional muscarinic receptors (Muscholl 1980).…”

mentioning

confidence: 99%

Lack of effect of topically applied nicotine on pial arteriole diameter and blood-brain barrier integrity in the cat

1992

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In the present study, the vasomotor effects of nicotine, its interaction with local chemical factors and norepinephrine, and its effects on the permeability of the blood-brain barrier (BBB) were investigated. Using perivascular microapplication, 10(-6) M nicotine was found not to exert a vasomotor effect by itself or to modify the vasodilating effect of an increase in perivascular H+, K+ and adenosine concentration. The constrictor effect of a decrease in H+, K+ or an increase in norepinephrine concentration in the perivascular space was also not altered by 10(-6) M nicotine, indicating a lack of interaction between nicotine and the compounds tested. Using cortical superfusion and intravital fluorescence microscopy nicotine (10(-7) to 10(-3) M) was also found not to affect the diameter of pial arteries during superfusion periods of 30 min each. The integrity of BBB could be demonstrated in time-matched solvent controls over 3 h using intravenously-infused FITC-labelled dextran (MW 70,000) as tracer. During cortical superfusion with 10(-7) to 10(-5) M nicotine the permeability of the BBB was not increased compared with the time-matched controls. However, during superfusion with 10(-4) and 10(-3) M nicotine, tracer extravasation could be quantified by computer-aided image analysis. The extravasation index (EI) increased by up to eight times. These data indicate that only toxic concentrations of nicotine increase BBB permeability to FITC-dextran 70,000.

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Inhibition of the Pial Artery Constriction Induced by Sympathetic Stimulation by Local Microapplication of a Cholinomimetic Agent

Cited by 8 publications

References 14 publications

Interaction between Cerebrovascular Sympathetic, Parasympathetic and Sensory Nerves in Blood Flow Regulation

Interaction between Cerebrovascular Sympathetic, Parasympathetic and Sensory Nerves in Blood Flow Regulation

Carbachol induces granular cell exocytosis and serotonin release in rabbit cerebral arteries

Lack of effect of topically applied nicotine on pial arteriole diameter and blood-brain barrier integrity in the cat

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