B. Hill et al., INNERVATION AND NITRIC-OXIDE MODULATION OF MESENTERIC-ARTERIES OF THEGOLDEN-HAMSTER, European journal of pharmacology, 317(2-3), 1996, pp. 275-283
Immunohistochemical and pharmacological techniques were used to examin
e perivascular nerves, endothelium and the effects of inhibition of ni
tric oxide synthesis on responses in mesenteric arteries/perfused mese
nteric arterial beds of the Golden hamster. Frequency-dependent vasoco
nstrictions to electrical field stimulation and dose-dependent vasocon
strictions to noradrenaline were significantly augmented by N-G-nitro-
L-arginine methyl ester (10(-5) M), an inhibitor of nitric oxide synth
ase. In preparations with tone raised with methoxamine (10 mu M) dose-
dependent relaxations to ATP, but not to acetylcholine, were blocked b
y N-G-nitro-L-arginine methyl ester. In the presence of guanethidine (
5 mu M) to block sympathetic neurotransmission there was no neurogenic
relaxation to electrical field stimulation. Furthermore, the sensory
neurotoxin capsaicin (0.05-5 nmol) did not elicit relaxation. Immunohi
stochemical studies demonstrated dense plexuses of fibres immunoreacti
ve for tyrosine hydroxylase and neuropeptide Y, a plexus of moderate d
ensity for calcitionin gene-related peptide and an absence of fibres i
mmunoreactive for substance P and vasoactive intestinal polypeptide. O
f particular interest is the finding that whereas sympathetic perivasc
ular nerves and nitric oxide regulate the function of hamster mesenter
ic arteries, there is no apparent motor function of calcitonin gene-re
lated peptide-containing sensory nerves.