当前位置： SCI文献检索 > ARCHIVES OF ORAL BIOLOGY期刊下所有文献 > Sympathectomy-induced increases in calcitonin gene-related peptide (CGRP)-, substance P- and vasoactive intestinal peptide (VIP)-levels in parotid and submandibular glands of the rat.

Sympathectomy-induced increases in calcitonin gene-related peptide (CGRP)-, substance P- and vasoactive intestinal peptide (VIP)-levels in parotid and submandibular glands of the rat.

Abstract：

:The neuropeptide contents of rat salivary glands were increased four weeks after sympathetic postganglionic denervation (but not after preganglionic denervation): calcitonin gene-related peptide (CGRP) by 400 and 65% in the parotid and submandibular glands, respectively; substance P by 30% in the submandibular gland; and vasoactive intestinal peptide (VIP) by 30% in the parotid gland. The sensory neurotoxin capsaicin prevented the expected increases of CGRP and substance P in the submandibular glands and of VIP in the parotid glands. The CGRP-increase in the parotid gland was, however, only reduced (by 65%). Parasympathetic otic ganglionectomy reduced the peptide levels in the parotid glands (CGRP--50%, VIP--98% and substance P--99%). From these residual levels, CGRP increased almost 8-fold and substance P 3-fold in response to the sympathetic denervation, while VIP was unaffected. In the parasympathetically denervated glands, the capsaicin-sensitive contribution to the CGRP-response to sympathetic denervation was roughly estimated to be more than 25% but less than 40%, while the corresponding contribution to the substance P-response was roughly estimated to be more than 6% but less than 58%. Most likely not only CGRP/substance P-containing sensory C-fibres (submandibular and parotid glands) but also parasympathetic VIP-containing secretomotor and vasomotor fibres (parotid glands) contributed to the capsaicin-sensitive response to sympathetic denervation.

journal_name

Arch Oral Biol

journal_title

Archives of oral biology

authors

Ekström J,Ekman R

doi

10.1016/j.archoralbio.2005.02.008

subject

Has Abstract

pub_date

2005-10-01 00:00:00

pages

909-17

issue

10

eissn

0003-9969

issn

1879-1506

pii

S0003-9969(05)00088-9

journal_volume

50

pub_type

杂志文章

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