Origins of nerve fibers containing nitric oxide synthase in the rat celiac-superior mesenteric ganglion

1995 ◽  
Vol 281 (2) ◽  
pp. 215-221 ◽  
Author(s):  
Tokio Domoto ◽  
Makoto Teramoto ◽  
Keiichiro Tanigawa ◽  
Katsuhiro Tamura ◽  
Yukihiko Yasui
1995 ◽  
Vol 281 (2) ◽  
pp. 215 ◽  
Author(s):  
Tokio Domoto ◽  
Makoto Teramoto ◽  
Keiichiro Tanigawa ◽  
Katsuhiro Tamura ◽  
Yukihiko Yasui

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

2009 ◽  
Vol 15 (4) ◽  
pp. 238-244
Author(s):  
A. Zahran ◽  
Hazem R. Ismail ◽  
S. Carrier ◽  
T. Hussein ◽  
P. Vachon

2014 ◽  
Vol 67 (9-10) ◽  
pp. 345-352 ◽  
Author(s):  
Sonja Smiljic ◽  
Vojkan Nestorovic ◽  
Sladjana Savic

Nitric oxide is produced by almost all cardiac cells, endothelial cells, cardiomyocytes and nerve fibers. It is synthesized by an enzyme, a nitric oxide synthase, which occurs in endothelial, neural and inducible form. The distribution of nitric oxide synthase in the heart is characterized by a pronounced non-uniformity. Nitric oxide exerts its effects in physiological and pathophysiological conditions. The physiological effects of low concentrations of nitric oxide, which is released in the normal conditions under the influence of constituent enzymes, occur via cyclic guanosine monophosphate. The synthesized nitric oxide exhibits its effect in the cells where it is produced, in an autocrine manner, or by diffusing into the neighboring cells, in a paracrine manner. Nitric oxide acts by regulating the coronary vessel tonus, affecting the contractility of cardiomyocytes, generating an inotropic effect in a dose-dependent manner and controlling the cellular respiration. Other effects of nitric oxide in the cardiovascular system include the hyperpolarization of the smooth muscle cells in blood vessels, the inhibition of the monocyte adhesion, the inhibition of platelet migration, adhesion and aggregation and the proliferation of smooth muscle cells and fibroblasts. The anti-atherosclerotic effects of nitric oxide are based on these effects. Nitric oxide is a weak free radical in gaseous state, and the cytotoxic and/or the cytoprotective effects of the higher concentrations of nitric oxide are related to the chemical structure of nitric oxide as a free radical. The excessive production of nitric oxide by the activation of inducible nitric oxide synthase can lead to major irregularities in the function of cardiomyocytes and cardiac insufficiency. Understanding the nitric oxide molecular mechanisms of signaling pathways in the heart can provide a new strategic approach to prevention and treatment of cardiovascular diseases.


1994 ◽  
Vol 275 (2) ◽  
pp. 355-360 ◽  
Author(s):  
Zarko Grozdanovic ◽  
Bernd Mayer ◽  
Hans Georg Baumgarten ◽  
Gerold Br�ning

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