Neurogenic vascular responses in male mouse mesenteric vascular beds.
Rat mesenteric arteries were maintained by both adrenergic vasoconstrictor nerves and calcitonin gene-related peptide (CGRP) vasodilator nerves. However, functions of these nerves in a pathophysiological state have not fully been analyzed. The use of disease models developed genetically in mice is expected to clarify neural function of perivascular nerves. Thus, we investigated basic mouse vascular responses. Mesenteric vascular beds isolated from male C57BL/6 mouse were perfused with Krebs solution and perfusion pressure was measured. Periarterial nerve stimulation (PNS, 8 - 24 Hz) induced frequency-dependent vasoconstriction, which increased flow rate-dependently. PNS-induced vasoconstriction was abolished by tetrodotoxin (neurotoxin) and guanethidine (adrenergic neuron blocker) and blunted by prazosin (α(1)-adrenoceptor antagonist). Injection of norepinephrine caused vasoconstriction, which was abolished by prazosin. In preparations with active tone, PNS (1 - 8 Hz) induced frequency-dependent vasodilation, which was inhibited by tetrodotoxin, capsaicin (CGRP depletor), and CGRP8-37 (CGRP-receptor antagonist). Injections of CGRP, acetylcholine, and sodium nitroprusside induced vasodilations. Vasodilator response to CGRP was inhibited by CGRP8-37. Immunohistochemical study showed innervation of tyrosine hydroxylase- and CGRP-immunopositive fibers in mesenteric arteries and veins. These results suggest that male mouse mesenteric vascular beds are useful for studying neural regulation of mesenteric arteries, which are innervated by adrenergic and CGRPergic nerves regulating vascular tone.
Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 1-1-1 Tsushima-naka, Okayama 700-8530, Japan.
Hiroki
H
Fujiwara
Narumi
N
Hashikawa-Hobara
Yoshihiro
Y
Wake
Shingo
S
Takatori
Mitsuhiro
M
Goda
Hiroshi
H
Higuchi
Yoshito
Y
Zamami
Panot
P
Tangsucharit
Hiromu
H
Kawasaki
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism / Q000494:pharmacology; D002211:Capsaicin / Q000494:pharmacology; D004195:Disease Models, Animal; D006145:Guanethidine / Q000494:pharmacology; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects* / Q000294:innervation* / Q000503:physiopathology; D051379:Mice; D008810:Mice, Inbred C57BL; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010446:Peptide Fragments / Q000494:pharmacology; D017933:Peripheral Nervous System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D011224:Prazosin / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D010446:Peptide Fragments; C058636:calcitonin gene-related peptide (8-37); D009599:Nitroprusside; D013779:Tetrodotoxin; D014446:Tyrosine 3-Monooxygenase; D015740:Calcitonin Gene-Related Peptide; D000109:Acetylcholine; D002211:Capsaicin; D009638:Norepinephrine; D011224:Prazosin; D006145:Guanethidine