Distribution and effects of neuropeptide Y, vasoactive intestinal peptide, substance P, and calcitonin gene-related peptide in human middle meningeal arteries: Comparison with cerebral and temporal arteries

Jansen, I.; Uddman, Rolf; Ekman, Rolf; Olesen, Jes; Ottosson, Anders; Edvinsson, Lars

doi:10.1016/0196-9781(92)90084-g

Cited by 100 publications

(64 citation statements)

References 43 publications

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“…Duckworth et al 10 reported an NE ED 50 of 7.9ϫ10 -7 mol/L in the proximal human MCA, Shibata 9.3ϫ10 -8 mol/L, 25 and Janson et al an ED 50 of 5.0Ϯ10 -7 mol/L. 26 Hardebo et al 27 concluded that the PA and STA were equally sensitive to NE, with a spread of values between 10 -6 and 10 -5 mol/L. These values are similar to the ED 50 values reported for other human arteries.…”

Section: Discussionmentioning

confidence: 99%

“…10 Nerve-induced dilation of PA has not been recorded in any animal species (see for example reference 12), although this is the dominant response in the proximal cerebral arteries of the cat 39 and pig. 41 A variety of dilator nerves have been visualized using different techniques in a number of species [42][43][44] : those containing ACh, 42,43 neuropeptide Y, vasoactive intestinal peptide, substance P, calcitonin gene-related peptide, [43][44][45] and NO. 46 Evidence for a functional role for some of these dilator neurotransmitters in nonhuman arteries has been reviewed.…”

Section: Discussionmentioning

confidence: 99%

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Weakness of Sympathetic Neural Control of Human Pial Compared With Superficial Temporal Arteries Reflects Low Innervation Density and Poor Sympathetic Responsiveness

Bevan

Dodge²,

Nichols³

et al. 1998

Stroke

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Background and Purpose-The primary goal of these studies was to understand and investigate the capacity of perivascular nerves to influence the tone of human pial arteries and to compare them with other human cephalic arteries, the superficial temporal and middle meningeal. Methods-Responses to electrical activation of intramural nerves and related features of fresh segments of human cephalic arteries-the pial (PA; 478Ϯ34 m ID), middle meningeal (MMA; 540Ϯ41 m ID), and superficial temporal (STA; 639Ϯ49 m ID)-obtained from patients aged 15 to 82 years during surgical procedures were studied on a resistance artery myograph. Results-The PA segment responses to electrical nerve activation and to norepinephrine (NE; 10 Ϫ5 mol/L) were 1% and 21% of tissue maximum, respectively, compared with 6% and 34% for the MMA and 14% and 90% for the STA. Tissue maximum was defined as the force increase to 127 mmol/L KCl plus arginine vasopressin (1 m). All arteries dilated well to acetylcholine. Possible explanations for the PA marginal neurogenic responses were assessed. NE ED 50 was 5.4Ϯ2.2ϫ10Ϫ7 mol/L and did not vary with age or diameter. NE responsiveness did not increase in vessels with spontaneous or raised potassium-induced tone. Relaxation to isoproterenol was variable and propranolol did not increase the neurogenic response. Neither N G -monomethyl-L-arginine, N G -nitro-L-arginine methyl ester, endothelium removal, nor indomethacin consistently influenced the contractions to NE or neurogenic reactivity. The weak PA neurogenic response is in keeping with its poor innervation. As determined by catecholamine histofluorescence, innervation in the PA is sparse, with density increasing in the order PA, MMA, and STA. The incidence of nerve structures in the PA adventitio-medial junction was only 3% of those in the STA, and these were situated more than 3 m from the closest smooth muscle cell. Conclusions-We conclude that the weak neurogenic response of adult human pial artery reflects its poor innervation and responsiveness to NE, implying that these features are not important in the regulation of its diameter. (Stroke. 1998;29:212-221.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Weakness of Sympathetic Neural Control of Human Pial Compared With Superficial Temporal Arteries Reflects Low Innervation Density and Poor Sympathetic Responsiveness

Bevan

Dodge²,

Nichols³

et al. 1998

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“…5 Isolated human pial arteries are approximately 10 times as sensitive to CGRP as middle meningeal arteries and 20 times as sensitive as subcutaneous arteries. 19 CGRP is present in perivascular trigeminal-nerve fibers that supply the pial arteries, the meningeal arteries, 20 and the extracranial cephalic arteries. 21 Stimulation of the trigeminal ganglion in humans and cats 22 and electrical stimulation of the superior sagittal sinus in animals 23,24 induce the release of CGRP into the cranial circulation.…”

Section: Tolerability and Safetymentioning

confidence: 99%

Calcitonin Gene–Related Peptide Receptor Antagonist BIBN 4096 BS for the Acute Treatment of Migraine

et al. 2004

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“…For example, feline pial arteries in situ dilated substantially to SP concentrations of 10" 9 to 10" 6 mol/L, 32 and the pD 2 for isolated human cerebral arteries was reported as 8.7. 33 Likewise, in vitro pD 2 values for CGRP of cerebral arteries of various species ranged from 8.3 to 9.4, with a maximum response at 10~7 mol/L. 8 - 34 Thus, according to our findings, the CSF peptide concentrations varied between levels inducing half-maximal (basal values) and maximal (30-minute values) relaxation.…”

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confidence: 96%

Time course of variations in rabbit cerebrospinal fluid levels of calcitonin gene-related peptide- and substance P-like immunoreactivity in experimental subarachnoid hemorrhage.

Dinh

Debdi

Couraud

et al. 1994

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Background and Purpose Cerebral vasospasm after subarachnoid hemorrhage may result partially from the imbalance between vasodilator and vasoconstrictor factors. The vasodilator peptides substance P and calcitonin gene-related peptide contained in the trigeminovascular system are involved in the vasomotor phenomenon occurring after subarachnoid hemorrhage. The delayed arterial narrowing may reflect the time course of the release of these peptides. Therefore, we followed the time course of the changes in cerebrospinal fluid immunoreactivity of substance P and calcitonin gene-related peptide in a model of experimental subarachnoid hemorrhage.Methods Cerebrospinal fluid samples were taken in the basal state and at 30 minutes, 24 hours, and 3 days after a single injection of 1 mL autologous arterial blood into the cisterna magna of rabbits using a percutaneous suboccipital route. Substance P-like and calcitonin gene-related peptidelike immunoreactivities were determined in centrifuged cerebrospinal fluid and plasma by use of enzyme immunoassay.Results Early (30 minutes) after induced subarachnoid hemorrhage, there was a large increase in cerebrospinal fluid

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Distribution and effects of neuropeptide Y, vasoactive intestinal peptide, substance P, and calcitonin gene-related peptide in human middle meningeal arteries: Comparison with cerebral and temporal arteries

Cited by 100 publications

References 43 publications

Weakness of Sympathetic Neural Control of Human Pial Compared With Superficial Temporal Arteries Reflects Low Innervation Density and Poor Sympathetic Responsiveness

Weakness of Sympathetic Neural Control of Human Pial Compared With Superficial Temporal Arteries Reflects Low Innervation Density and Poor Sympathetic Responsiveness

Calcitonin Gene–Related Peptide Receptor Antagonist BIBN 4096 BS for the Acute Treatment of Migraine

Time course of variations in rabbit cerebrospinal fluid levels of calcitonin gene-related peptide- and substance P-like immunoreactivity in experimental subarachnoid hemorrhage.

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