Vasoactive intestinal peptide- and nitric oxide synthase-containing nerve fibers in the rat ophthalmic artery have different origins

1996 ◽  
Vol 234 (2) ◽  
pp. 125-130 ◽  
Author(s):  
Tor Elsås ◽  
Rolf Uddman ◽  
Frank Sundler
1997 ◽  
Vol 17 (9) ◽  
pp. 977-984 ◽  
Author(s):  
Carmen González ◽  
Carla Barroso ◽  
Carmen Martín ◽  
Sergio Gulbenkian ◽  
Carmen Estrada

The participation of nitric oxide and vasoactive intestinal peptide (VIP) in the neurogenic regulation of bovine cerebral arteries was investigated. Nitrergic nerve fibers and ganglion-like groups of neurons were revealed by NADPH-diaphorase staining in the adventitial layer of bovine cerebral arteries. NADPH diaphorase also was present in endothelial cells but not in the smooth muscle layer. Double immunolabeling for neuronal nitric oxide synthase and VIP indicated that both molecules co-localized in the same nerve fibers in these vessels. Transmural nerve stimulation (200 mA, 0.2 milliseconds, 1 to 8 Hz) of endothelium-denuded bovine cerebral artery rings precontracted with prostaglandin F2α, produced tetrodotoxin-sensitive relaxations that were completely suppressed by NG-nitro-l-arginine methyl ester (l-NAME) and by the guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline (ODQ), but were not affected by the adenylyl cyclase inhibitor 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), nor by VIP tachyphylaxis induced by pretreatment with 1 μmol/L VIP. Transmural nerve stimulation also elicited increases in intracellular cyclic GMP concentration, which were prevented by l-NAME, and small decreases in intracellular cyclic AMP concentration. Addition of VIP to bovine cerebral artery rings without endothelium produced a concentration-dependent relaxation that was partially inhibited by l-NAME, ODQ, and SQ 22,536. The effects of l-NAME and SQ 22,536 were additive. VIP induced a transient increase in intracellular cyclic GMP concentration, which was maximal 1 minute after VIP addition, when the highest relaxation rate was observed, and which was blocked by l-NAME. It is concluded that nitric oxide produced by perivascular neurons and nerve fibers fully accounts for the experimental neurogenic relaxation of bovine cerebral arteries and that VIP, which also is present in the same perivascular fibers, acts as a neuromodulator by activating neuronal nitric oxide synthase.


1994 ◽  
Vol 111 (4) ◽  
pp. 430-438 ◽  
Author(s):  
Andrew Harper ◽  
William R. Blythe ◽  
Carlton J. Zdanski ◽  
Jiri Prazma ◽  
Harold C. Pillsbury

Nitric oxide is known to function as a neurotransmitter in the central nervous system. It is also known to be involved in the control nervous system excitatory amino acid neurotransmission cascade. Activation of excitatory amino acid receptors causes an influx of calcium, which activates nitric oxide synthase. The resulting increase in intracellular nitric oxide activates soluble guanylate cyclase, leading to a rise in cyclic guanosine monophosphate. The excitatory amino acids giutamate and aspartate are found in the vestibular system and have been postulated to function as vestibular system neurotransmitters. Although nitric oxide has ben investigated as a neurotransmitter in other tissues, no published studies have examined the role of nitric oxide in the vestibular system. Neuronal NADPH-dlaphorase has been characterized as a nitric oxide synthase. This enzyme catalyzes the conversion of L-arginine to l-citrulline, producing nitric oxide during the reaction. We used a histochemical stain characterized by Hope et al. (Proc Natl Acad Sci 1991;88:2811) as specific for neuronal nitric oxide synthase to localize the enzyme in the rat vestibular system. An Immunocytochemical stain was used to examine rat Inner ear tissue for the presence of the enzyme's end product, l-citrulline, thereby demonstrating nitric oxide synthase activity. Staining of vestibular ganglion sections showed nitric oxide synthase presence and activity in ganglion cells and nerve fibers. These results Indicate the presence of active nitric oxide synthase in these tissues and suggest modulation of vestibular neurotransmission by nitric oxide.


1996 ◽  
Vol 738 (2) ◽  
pp. 292-300 ◽  
Author(s):  
N.J. Dun ◽  
S.L. Dun ◽  
R.L. Huang ◽  
E.C. Dun ◽  
C.C. Lai ◽  
...  

1994 ◽  
Vol 657 (1-2) ◽  
pp. 7-13 ◽  
Author(s):  
Toyoyuki Hanazawa ◽  
Akiyoshi Konno ◽  
Toshio Kaneko ◽  
Koichi Tanaka ◽  
Hiroshi Ohshima ◽  
...  

1993 ◽  
Vol 18 ◽  
pp. S65
Author(s):  
Toyoyuki Hanazawa ◽  
Koichi Tanaka ◽  
Hiroshi Ohshima ◽  
Hiroyasu Esumi ◽  
Tanemichi Chiba

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