Innervation and nitric oxide modulation of mesenteric arteries of the golden hamster.

Immunohistochemical and pharmacological techniques were used to examine perivascular nerves, endothelium and the effects of inhibition of nitric oxide synthesis on responses in mesenteric arteries/perfused mesenteric arterial beds of the Golden hamster. Frequency-dependent vasoconstrictions to electrical field stimulation and dose-dependent vasoconstrictions to noradrenaline were significantly augmented by NG-nitro-L-arginine methyl ester (10(-5) M), an inhibitor of nitric oxide synthase. In preparations with tone raised with methoxamine (10 microM) dose-dependent relaxations to ATP, but not to acetylcholine, were blocked by NG-nitro-L-arginine methyl ester. In the presence of guanethidine (5 microM) 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. Immunohistochemical studies demonstrated dense plexuses of fibres immunoreactive for tyrosine hydroxylase and neuropeptide Y, a plexus of moderate density for calcitionin gene-related peptide and an absence of fibres immunoreactive for substance P and vasoactive intestinal polypeptide. Of particular interest is the finding that whereas sympathetic perivascular nerves and nitric oxide regulate the function of hamster mesenteric arteries, there is no apparent motor function of calcitonin gene-related peptide-containing sensory nerves.