TY - JOUR
T1 - Endothelin localizes in the dorsal horn and acts on the spinal neurones
T2 - Possible involvement of dihydropyridine-sensitive calcium channels and substance P release
AU - Yoshizawa, Toshihiro
AU - Kimura, Sadao
AU - Kanazawa, Ichiro
AU - Uchiyama, Yasuo
AU - Yanagisawa, Masashi
AU - Masaki, Tomoh
N1 - Funding Information:
We wish to thank Professor M. Otsuka, Tokyo Medical and Dental University, for his valuable criticism and encouragement. This work was supported in part by a grant from Scientific Research on Priority Areas, Ministry of Education, Science and Culture, Japan.
PY - 1989/7/31
Y1 - 1989/7/31
N2 - The neural effect of endothelin, a vasoconstrictor peptide from vascular endothelium, was investigated in the in vitro spinal cord preparation of the newborn rat. In addition, an immunohistochemical study of endothelin was performed in the porcine spinal cord. Endothelin produced ventral root depolarization in a dose-dependent manner in the newborn rat spinal cord. Endothelin (5 × 10-8 M)-induced depolarization was depressed by the dihydropyridine-sensitive Ca2+ channel blocker, nicardipine (10-7 M), or the substance P antagonist, spantide (5 × 10-6 M). These results suggest that endothelin may cause substance P release and that dihydropyridine-sensitive Ca2+ channels in the spinal cord may be involved in this process. Furthermore, endothelin-like immunoreactivity was localized in dot- and fibre-like structures and neurones in the dorsal horn of the porcine spinal cord. Therefore, it is suggested that endothelin or endothelin-related peptide(s) have a neuromodulatory function in the spinal cord.
AB - The neural effect of endothelin, a vasoconstrictor peptide from vascular endothelium, was investigated in the in vitro spinal cord preparation of the newborn rat. In addition, an immunohistochemical study of endothelin was performed in the porcine spinal cord. Endothelin produced ventral root depolarization in a dose-dependent manner in the newborn rat spinal cord. Endothelin (5 × 10-8 M)-induced depolarization was depressed by the dihydropyridine-sensitive Ca2+ channel blocker, nicardipine (10-7 M), or the substance P antagonist, spantide (5 × 10-6 M). These results suggest that endothelin may cause substance P release and that dihydropyridine-sensitive Ca2+ channels in the spinal cord may be involved in this process. Furthermore, endothelin-like immunoreactivity was localized in dot- and fibre-like structures and neurones in the dorsal horn of the porcine spinal cord. Therefore, it is suggested that endothelin or endothelin-related peptide(s) have a neuromodulatory function in the spinal cord.
KW - Dihydropyridine-sensitive calcium channel
KW - Endothelin
KW - Immunohistochemistry
KW - Nicardipine
KW - Spinal cord
KW - Substance P
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U2 - 10.1016/0304-3940(89)90075-X
DO - 10.1016/0304-3940(89)90075-X
M3 - Article
C2 - 2478929
AN - SCOPUS:0024338868
SN - 0304-3940
VL - 102
SP - 179
EP - 184
JO - Neuroscience letters
JF - Neuroscience letters
IS - 2-3
ER -