Nitric oxide as a mediator of parasympathetic vasodilation in ocular and extraocular tissues in the rabbit.
OBJECTIVE
The aim of this study was to investigate in rabbits the relationship between nitric oxide and the noncholinergic vasodilation caused by facial nerve stimulation in the eye and some extraocular tissues.


METHODS
Uveal vascular resistance was determined by measuring simultaneously the flow from a cannulated vortex vein with intraocular pressure and arterial blood pressure recordings. The local blood flow in different parts of the eye (iris, ciliary body, choroid, and retina), eyelids, nictitating membrane, Harderian gland, and lacrimal gland was determined using radioactive microspheres. The effects of facial nerve stimulation, at different frequencies, were examined before and after the administration of nitric oxide synthase (NOS) inhibitors.


RESULTS
In the experiments with direct determination of uveal blood flow, stimulation of the facial nerve caused a frequency-dependent decrease in uveal vascular resistance, indicating vasodilation. This effect was reduced or abolished by NOS inhibition at low frequencies but was unaffected at high frequencies. Determination of regional blood flow, with radioactive microspheres, showed that the stimulation increased local blood flow in all parts of the uvea. Compared to the nonstimulated control side, stimulation at 2 Hz increased choroidal blood flow by 89% +/- 12% before NOS inhibition and by 45% +/- 10% after NOS inhibition, a difference of 44% +/- 77% (n = 9; P < or = 0.05). Iris and ciliary body vasodilation appeared to be equally reduced. In eyelids, Harderian gland, and lacrimal gland, the vasodilation elicited by stimulation at 2 Hz was abolished almost completely by NOS inhibition. The vasodilation in most of the extraocular tissues was reduced significantly by NOS inhibition at 5 Hz, with only a slight reduction in the choroid, iris, and ciliary body. Retinal blood flow also was significantly increased by facial nerve stimulation at 2 Hz and 5 Hz. The increase in retinal blood flow appeared to be more sensitive to NOS inhibition than the increase in uveal blood flow.


CONCLUSIONS
These results suggest that the formation of nitric oxide plays an important role in the uveal, retinal, and extraocular vasodilation brought about by facial nerve stimulation at low frequencies. At high frequencies, other neurotransmitters also seem to be involved.
Nilsson
S F
SF
Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects; D001808:Blood Vessels / Q000294:innervation; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005123:Eye / Q000098:blood supply* / Q000294:innervation; D005154:Facial Nerve / Q000187:drug effects / Q000502:physiology; D005260:Female; D006243:Harderian Gland / Q000098:blood supply; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine; D010275:Parasympathetic Nervous System / Q000502:physiology*; D011817:Rabbits; D012039:Regional Blood Flow; D014602:Uvea / Q000098:blood supply / Q000294:innervation; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
D004791:Enzyme Inhibitors; D019335:Nitroarginine; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester