title: Modulation by neurogenic acetylcholine of nitroxidergic nerve function in porcine ciliary arteries.
abstract: OBJECTIVE
  To determine whether nitroxidergic, cholinergic, and vasoactive intestinal polypeptide (VIP)-mediated nerves participate in the regulation of porcine ciliary arterial tone and to analyze the mechanisms underlying the neuronal interaction.
  
  
  METHODS
  Changes in isometric tension were recorded in helical strips of the arteries, which were stimulated by transmurally applied electrical pulses or nicotine. The presence of perivascular nerve fibers containing reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase, acetylcholinesterase, and VIP immunoreactivity were determined histologically.
  
  
  RESULTS
  Transmural electrical stimulation (2, 5, and 20 Hz) and nicotine produced a relaxation of the arterial strips denuded of the endothelium and contracted with prostaglandin F2alpha. The response was not influenced by timolol but was abolished by oxyhemoglobin and methylene blue. N(G)-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor, abolished the neurogenic relaxation, and L-arginine restored the response. Physostigmine inhibited, but atropine potentiated, the neurogenic response. The relaxation was attenuated by acetylcholine but was not influenced by VIP. There were nerve fibers and bundles containing NADPH diaphorase, acetylcholinesterase, and VIP immunoreactivity in the adventitia of ciliary arteries.
  
  
  CONCLUSIONS
  Porcine ciliary arteries are innervated by NO synthase-containing nerves that liberate NO, possibly as a neurotransmitter on excitation to produce muscular relaxation. Nitroxidergic nerve function is inhibited by acetylcholine released from cholinergic nerve, possibly because of impaired production or release of NO. VIP does not seem to function as a neurotransmitter or a modulator.
authors.affiliation: Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Toda
authors.forename: T
authors.initials: T
authors.lastname: Okamura
authors.forename: I
authors.initials: I
authors.lastname: Azuma
authors.forename: N
authors.initials: N
authors.lastname: Toda
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D002799:Cholinergic Fibers / Q000187:drug effects / Q000502:physiology*; D019842:Ciliary Arteries / Q000187:drug effects / Q000294:innervation*; D004558:Electric Stimulation; D005260:Female; D007124:Immunoenzyme Techniques; D007537:Isometric Contraction / Q000187:drug effects; D008297:Male; D009126:Muscle Relaxation / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009252:NADPH Dehydrogenase / Q000378:metabolism; D009538:Nicotine / Q000494:pharmacology; D018722:Nicotinic Agonists / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D013552:Swine; D014660:Vasoactive Intestinal Peptide / Q000378:metabolism
chemical_list: D018722:Nicotinic Agonists; D009569:Nitric Oxide; D014660:Vasoactive Intestinal Peptide; D009538:Nicotine; D019001:Nitric Oxide Synthase; D009252:NADPH Dehydrogenase; D000110:Acetylcholinesterase; D000109:Acetylcholine