Non-adrenergic non-chlinergic (NANC) inhibition in longitudinal smooth muscle of rat jejunum: Minor role of nitric oxide (NO)

1998 ◽  
Vol 114 ◽  
pp. A716 ◽  
Author(s):  
B.M. Balsiger ◽  
N. Ohtani ◽  
C. Shibata ◽  
M.G. Sarr
2007 ◽  
Vol 141 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Michael S. Kasparek ◽  
Javairiah Fatima ◽  
Corey W. Iqbal ◽  
Judith A. Duenes ◽  
Michael G. Sarr

2013 ◽  
Vol 65 ◽  
pp. S104
Author(s):  
Manuel Alejandro Ramirez-Lee ◽  
Hector Rosas-Hernandez ◽  
Samuel Salazar-Garcia ◽  
Jose Manuel Gutiérrez-Hernández ◽  
Ricardo Espinosa- Tanguma ◽  
...  

1998 ◽  
Vol 274 (2) ◽  
pp. G306-G313 ◽  
Author(s):  
Simon A. Ahtaridis ◽  
Surender S. Katoch ◽  
Robert S. Moreland

Intact and α-toxin-permeabilized longitudinal smooth muscle were mounted for measurement of force and myosin light chain phosphorylation. Galanin contracted intact jejunum with a half-maximum effective concentration of 9.2 ± 0.1 nM. Neither atropine, hexamethonium, guanethidine, nor tetrodotoxin affected the contraction. The contraction was also unaffected by depletion of intracellular Ca2+ or by addition of thapsigargin; removal of extracellular Ca2+ or addition of nifedipine abolished the contraction. Galanin increased myosin light chain phosphorylation levels concomitantly with force. During continued tissue stimulation, force fell to suprabasal values, whereas myosin light chain phosphorylation levels remained elevated. Galanin increased Ca2+ sensitivity of contraction in α-toxin-permeabilized tissues, and this was reversed by either guanosine 5′- O-(2-thiodiphosphate) or pertussis toxin. These results suggest that galanin-induced contraction of longitudinal jejunal smooth muscle is dependent on a pertussis toxin-sensitive G protein that is apparently not coupled to the release of intracellular Ca2+but to the influx of extracellular Ca2+ and involves an initial myofilament Ca2+ sensitization followed by Ca2+ desensitization.


1995 ◽  
Vol 110 (1) ◽  
pp. 157-164 ◽  
Author(s):  
William G. Richards ◽  
Jonathan S. Stamler ◽  
Lester Kobzik ◽  
David J. Sugarbaker

2019 ◽  
Vol 31 (1) ◽  
pp. 63-71 ◽  
Author(s):  
Michelle Alexandra Mistry ◽  
Niels Klarskov ◽  
John O. DeLancey ◽  
Gunnar Lose

1996 ◽  
Vol 5 (1) ◽  
pp. 62-68 ◽  
Author(s):  
Dominique Vaillier ◽  
Richard Daculsi ◽  
Norbert Gualdel

The production of nitric oxide (NO) was measured in cultures of spleen cells stimulated by lipopolysaccharide (LPS), IL-2 or LPS + IL-2. We observed that NO synthesis is increased by IFN-γ but inhibited by IFN-α/β. This is not the case when IL-2 is present in the cultures, since interferons play a minor role in the regulation of the NO production. When IL-2 and LPS were associated in the cultures, the IFN-α/β role seems more important than that of IFN-γ. PGE2inhibits NO production in LPS supplemented cultures but has a slight effect in the presence of IL-2 and no effect with IL-2 + LPS. 3-isoButyl-1-methylxanthine (IBMX), an inhibitor of phosphodiesterases, induces a decrease of IFN production. In the presence of H-7, an inhibitor of protein kinase C (PKC), NO production is reduced when the cultures are supplemented by LPS or IL-2 but not when IL-2 and LPS are both added. H-7 also reduced IFN production. In the presence of NG-monomethyl-L-arginine (N-MMA), an inhibitor of NO synthesis, IFN production was increased, with no change in the cytotoxic activity. Hence, interferons regulate NO production by mouse spleen cells and, in return, NO modulates the generation of IFN.


2011 ◽  
Vol 207 (3) ◽  
pp. 306-313 ◽  
Author(s):  
Carmen González ◽  
Samuel Salazar-García ◽  
Gabriela Palestino ◽  
Pedro P. Martínez-Cuevas ◽  
Manuel A. Ramírez-Lee ◽  
...  

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