The peptidergic innervation of the human superficial temporal artery: immunohistochemistry, ultrastructure, and vasomotility.
The peptidergic innervation of the human superficial temporal artery was investigated by means of immunohistochemical, ultrastructural, and in vitro pharmacological techniques. A dense network of nerve fibers was found in the adventitia. The majority of the nerve fibers displayed immunoreactivity for tyrosine hydroxylase and neuropeptide Y (NPY). A moderate supply of perivascular nerve fibers displayed either acetylcholinesterase activity or immunoreactivity for vasoactive intestinal peptide (VIP), peptide histidine methionine-27 (PHM), and calcitonin gene-related peptide (CGRP). Only a few nerve fibers displayed substance P (SP), neurokinin A (NKA), and neuropeptide K (NPK) immunoreactivity. In double immunostained preparations, SP immunoreactivity was co-localized with NPK and CGRP in the same nerve fibers. Ultrastructural studies revealed the presence of numerous axon variocosities at the adventitial--medial border. NPY, VIP, and CGRP immunoreactivities occurred in the same type of large granular vesicles, but in morphological distinct nerve profiles. NPY had, in general, no direct vasoconstrictor effect. However, at a low concentration of NPY contractile response induced by NA (10(-7)-10(-6)M) was 9-15 times enhanced. The NPY-induced potentiation of the NA-induced contraction was not dependent on the presence of an intact endothelium. No significant difference was found between acetylcholine, VIP, and PHM in either potency or degree of relaxation. SP, NKA, and CGRP also acted as vasodilatory agents, with CGRP being more potent than the tachykinins. The response to SP, but not CGRP, was dependent on an intact endothelium. Pretreatment of the vessels with a low concentration of NPY did not change the responses to ACh, VIP, SP, or CGRP.
Olesen
I J
IJ
Department of Experimental Research, Lund University, Malmö General Hospital, Sweden.
Gulbenkian
S
S
Valença
A
A
Antunes
J L
JL
Wharton
J
J
Polak
J M
JM
Edvinsson
L
L
D000110:Acetylcholinesterase / Q000032:analysis; D000818:Animals; D000906:Antibodies; D015740:Calcitonin Gene-Related Peptide / Q000032:analysis; D005455:Fluorescent Antibody Technique; D006801:Humans; D008854:Microscopy, Electron; D016253:Microscopy, Immunoelectron; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000294:innervation / Q000502:physiology / Q000648:ultrastructure; D009412:Nerve Fibers / Q000648:ultrastructure*; D015288:Neurokinin A / Q000032:analysis; D009478:Neuropeptide Y / Q000032:analysis; D009479:Neuropeptides / Q000032:analysis; D010451:Peptide PHI / Q000032:analysis; D011817:Rabbits / Q000276:immunology; D051381:Rats / Q000276:immunology; D013373:Substance P / Q000032:analysis; D015320:Tachykinins; D013699:Temporal Arteries / Q000294:innervation* / Q000502:physiology / Q000648:ultrastructure; D014446:Tyrosine 3-Monooxygenase / Q000032:analysis; D014660:Vasoactive Intestinal Peptide / Q000032:analysis
D000906:Antibodies; D009478:Neuropeptide Y; D009479:Neuropeptides; D010451:Peptide PHI; D015320:Tachykinins; C045206:neuropeptide K; D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D015288:Neurokinin A; D014446:Tyrosine 3-Monooxygenase; D000110:Acetylcholinesterase; D015740:Calcitonin Gene-Related Peptide