RELATIONSHIPS BETWEEN PERMEABLE VESSELS, NERVES, AND MAST-CELLS IN RAT CUTANEOUS NEUROGENIC INFLAMMATION

被引:39
作者
BARANIUK, JN [1 ]
KOWALSKI, ML [1 ]
KALINER, MA [1 ]
机构
[1] NIAID,CLIN INVEST LAB,ALLERG DIS SECT,BETHESDA,MD 20892
关键词
calcitonin gene-related peptide; Monastral blue B; neurokinin A; substance P; vascular permeability; vasodilation;
D O I
10.1152/jappl.1990.68.6.2305
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Electrical stimulation of rat sensory nerves produces cutaneous vasodilation and plasma protein extravasation, a phenomenon termed 'neurogenic inflammation'. Rat skin on the dorsum of the paw developed neurogenic inflammation after electrical stimulation of the saphenous nerve. In tissue sections, the extravasation of the supravital dye Monastral blue B identified permeable vessels. Mast cells were identified by toluidine blue stain. Permeable vessels were significantly more dense in the superficial 120 μm of the dermis than in the deeper dermis, whereas mast cells were significantly more frequent in the deeper dermis. The relationships between nociceptive sensory nerve fibers, permeable vessels, and mast cells were examined by indirect immunohistochemistry for calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and substance P (SP). CGRP-, NKA-, and SP-containing nerves densely innervated the superficial dermis and appeared to innervate the vessels that became permeable during neurogenic inflammation. In contrast, mast cells were not associated with either permeable vessels or nerve fibers. These data suggest that electrical stimulation of rat sensory nerves produces vascular permeability by inducing the release of neuropeptides that may directly stimulate the superficial vascular bed. Mast cells may not be involved in this stage of cutaneous neurogenic inflammation in rat skin.
引用
收藏
页码:2305 / 2311
页数:7
相关论文
共 49 条
[1]   HISTAMINE IS RELEASED FROM SKIN BY SUBSTANCE-P BUT DOES NOT ACT AS THE FINAL VASODILATOR IN THE AXON REFLEX [J].
BARNES, PJ ;
BROWN, MJ ;
DOLLERY, CT ;
FULLER, RW ;
HEAVEY, DJ ;
IND, PW .
BRITISH JOURNAL OF PHARMACOLOGY, 1986, 88 (04) :741-745
[2]  
Bayliss WM, 1901, J PHYSIOL-LONDON, V26, P173
[3]   INFLAMMATORY EDEMA INDUCED BY SYNERGISM BETWEEN CALCITONIN GENE-RELATED PEPTIDE (CGRP) AND MEDIATORS OF INCREASED VASCULAR-PERMEABILITY [J].
BRAIN, SD ;
WILLIAMS, TJ .
BRITISH JOURNAL OF PHARMACOLOGY, 1985, 86 (04) :855-860
[4]   SUBSTANCE-P REGULATES THE VASODILATOR ACTIVITY OF CALCITONIN GENE-RELATED PEPTIDE [J].
BRAIN, SD ;
WILLIAMS, TJ .
NATURE, 1988, 335 (6185) :73-75
[5]   POTENT VASODILATOR ACTIVITY OF CALCITONIN GENE-RELATED PEPTIDE IN HUMAN-SKIN [J].
BRAIN, SD ;
TIPPINS, JR ;
MORRIS, HR ;
MACINTYRE, I ;
WILLIAMS, TJ .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1986, 87 (04) :533-536
[6]   ANTIDROMIC VASODILATATION AND NEUROGENIC INFLAMMATION [J].
CHAHL, LA .
PHARMACOLOGY & THERAPEUTICS, 1988, 37 (02) :275-300
[7]  
DASILVA AR, 1988, REGUL PEPTIDES, V88, P22
[8]   ROLE OF THE N-TERMINAL ARGININE IN THE HISTAMINE-RELEASING ACTIVITY OF SUBSTANCE-P, BRADYKININ AND RELATED PEPTIDES [J].
DEVILLIER, P ;
DRAPEAU, G ;
RENOUX, M ;
REGOLI, D .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1989, 168 (01) :53-60
[9]  
ENERBACK L, 1987, ALLERGY INFLAMMATION, P351
[10]   HISTAMINE-RELEASE AND VASCULAR CHANGES INDUCED BY NEUROPEPTIDES [J].
FOREMAN, J ;
JORDAN, C .
AGENTS AND ACTIONS, 1983, 13 (2-3) :105-116