scholarly journals Innervation Pattern of Substance P- and Calcitonin Gene-related Peptide-Immunoreactive Nerves of the Cerebral Arteries in the Quail

2000 ◽  
Vol 62 (6) ◽  
pp. 595-602 ◽  
Author(s):  
Haruo KUSABA ◽  
Koichi ANDO ◽  
Noboru FUJIHARA
Keyword(s):  
Substance P ◽  
Cerebral Arteries ◽  
Calcitonin Gene Related Peptide ◽  
Innervation Pattern ◽  
Related Peptide ◽  
Calcitonin Gene

Effects of neuropeptide Y, calcitonin gene-related peptide, substance P, and capsaicin on cerebral arteries in man and animals

1988 ◽  
Vol 69 (6) ◽  
pp. 913-918 ◽  
Author(s):  
Juan Armando Mejia ◽  
John Pernow ◽  
Hans von Holst ◽  
Anders Rudehill ◽  
Jan M. Lundberg
Keyword(s):  
Substance P ◽  
Neuropeptide Y ◽  
Muscle Tone ◽  
Cerebral Arteries ◽  
Calcitonin Gene Related Peptide ◽  
Sensory Nerves ◽  
Pial Arteries ◽  
Relaxant Effect ◽  
Related Peptide ◽  
Calcitonin Gene

✓ The smooth-muscle tone of pial, middle, and anterior cerebral arteries from humans, cats, and pigs, respectively, was studied in vitro with respect to the effects of capsaicin and various peptides which are present in local perivascular nerves. Neuropeptide Y (NPY) caused concentration-dependent, potent contractions of the cerebral vessels both in the presence and in the absence of endothelium. In contrast to the response to noradrenaline (NA) and K+, the NPY effect was not altered by changes in the extracellular Ca++ concentration. The relaxant action of the calcium antagonist nifedipine on NPY-evoked contraction of cerebral arteries was not inhibited by a Ca++-deficient medium or by a high-Ca++ medium. Calcitonin gene-related peptide (CGRP), substance P (SP), and capsaicin caused relaxation of precontracted cerebral arteries with an intact endothelium. Calcitonin gene-related peptide was the most potent dilatory agent, and removal of the endothelium did not change the CGRP response. In contrast, the ability of SP to cause relaxation was abolished after removal of the endothelium. Capsaicin, which activates sensory nerves, induced long-lasting relaxation in both the presence and absence of endothelium. In conclusion, in contrast to earlier reported data, the contractile effect of NPY seems to be largely independent of extracellular Ca++, while NA- and K+-induced contractions are dependent on extracellular Ca++. The present results suggest that the relaxant effect of nifedipine on cerebral blood vessels may involve actions other than inhibition of Ca++ influx. The relaxant effect of capsaicin is likely to be induced by release of CGRP rather than SP. The potent effects of these peptides on human pial arteries suggest that neuropeptides may be involved in the control of cerebral blood flow in man.

Twenty six-week repeat dose oral rat toxicity study of cizolirtine, a substance-P and calcitonin gene-related peptide release modulator

2021 ◽  
Vol 122 ◽  
pp. 104916
Author(s):  
Antonio Guzmán ◽  
Gregorio Encina ◽  
Antonio R. Fernández de Henestrosa ◽  
Cristina Vila ◽  
Araceli Tortajada ◽  
...  
Keyword(s):  
Substance P ◽  
Calcitonin Gene Related Peptide ◽  
Toxicity Study ◽  
Repeat Dose ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Peptide Release ◽  
Dose Oral

Release of Histamine from Dural Mast Cells by Substance P and Calcitonin Gene-Related Peptide

Cephalalgia ◽  
1997 ◽  
Vol 17 (3) ◽  
pp. 166-174 ◽  
Author(s):  
A Ottosson ◽  
L Edvinsson
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Histamine Release ◽  
Dura Mater ◽  
Neurogenic Inflammation ◽  
Calcitonin Gene Related Peptide ◽  
Sampling Procedure ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Peritoneal Mast Cells

The aim of the present study was to examine if the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) can stimulate histamine release from mast cells in the dura mater and thereby play a role in cranial vasoregulation and local neurogenic inflammation. Dura mater mast cells were compared with peritoneal mast cells in the rat. Histamine was released from dura mater mast cells by compound 48/80, SP and CGRP but from peritoneal mast cells only by compound 8/80 and SP. NPY and VIP released quite small amounts of histamine from dural mast cells. The release on SP and CGRP from rat dura mater mast cells was blocked by the receptor antagonists FK888 and CGRP8-37 respectively, suggesting receptor mediated release mechanisms. None of the stimuli released histamine from human or porcine dural mast cells, possibly because the sampling procedure injures and incapacitates the cells.

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