scholarly journals Non-adrenergic vasoconstriction and vasodilatation of guinea-pig aorta by β-phenylethylamine and amphetamine – Role of nitric oxide determined with L-NAME and NO scavengers

2018 ◽  
Vol 818 ◽  
pp. 198-205 ◽  
Author(s):  
Kenneth J. Broadley ◽  
Harrison D. Broadley
2013 ◽  
Vol 25 (2) ◽  
pp. e114-e126 ◽  
Author(s):  
C. Giaroni ◽  
S. Marchet ◽  
E. Carpanese ◽  
V. Prandoni ◽  
R. Oldrini ◽  
...  

2003 ◽  
Vol 285 (4) ◽  
pp. G747-G753 ◽  
Author(s):  
Catalina Caballero-Alomar ◽  
Carmen Santos ◽  
Diego Lopez ◽  
M. Teresa Mitjavila ◽  
Pere Puig-Parellada

We examined in vitro the source and role of basal nitric oxide (NO) in proximal segments of guinea pig taenia caeci in nonadrenergic, noncholinergic (NANC) conditions. Using electron paramagnetic resonance (EPR), we measured the effect of the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10–4 M), the neuronal blocker tetrodotoxin (TTX, 10–6 M), or both on spontaneous contractions and on the production of basal NO. Both l-NAME and TTX, when tested alone, increased the amplitude and frequency of contractions. NO production was abolished by l-NAME and was inhibited by 38% by TTX. When tested together, l-NAME in the presence of TTX or TTX in the presence of l-NAME had no further effect on the amplitude or frequency of spontaneous contractions, and the NO production was inhibited. These findings suggest that basal NO consists of TTX-sensitive and TTX-resistant components. The TTX-sensitive NO has an inhibitory effect on spontaneous contractions; the role of TTX-resistant NO is unknown.


Author(s):  
MichelR. Briejer ◽  
LouisM.A. Akkermans ◽  
AnnL. Meulemans ◽  
RomainA. Lefebvre ◽  
JanA.J. Schuurkes

1994 ◽  
Vol 251 (2-3) ◽  
pp. 221-227 ◽  
Author(s):  
Nagao Suzuki ◽  
Ken Mizuno ◽  
Yasuo Gomi

1995 ◽  
Vol 268 (6) ◽  
pp. G933-G942 ◽  
Author(s):  
A. Yanaka ◽  
H. Muto ◽  
H. Fukutomi ◽  
S. Ito ◽  
W. Silen

The role of nitric oxide (NO) in restitution was examined in intact sheets of in vitro guinea pig gastric mucosae after mucosal injury induced by exposure of the luminal surface to 1.25 M NaCl for 10 min. The recovery of transmucosal electrical resistance and [3H]mannitol flux after the injury were significantly greater at luminal pH (pH1) 7.0 than 3.0. The recovery was abolished by pretreatment with 1 mM NG-nitro-L-arginine methyl ester (L-NAME), only at pHL 3.0, an effect reversed by 1 mM L-arginine. Enhancement of the recovery by L-arginine at pHL 3.0 was abolished by 50 microM methylene blue (MB), an effect restored by 1 mM N6,2'-O-dibutyryl guanosine 3',5'-cyclic monophosphate (DBcGMP). In L-arginine- but not L-NAME-treated tissues, recovery was enhanced further by an increase in serosal [HCO3-] and was inhibited by 5% N-acetyl-L-cysteine in the luminal solution or by the removal of serosal HCO3-. Morphological examination showed the formation of a thick "mucoid cap" in L-arginine-but not L-NAME-treated tissues. These results suggest that, in the presence of luminal acid, endogenous NO contributes to restitution in injured gastric mucosa at least in part by facilitating the formation of the mucoid cap.


1999 ◽  
Vol 380 (1) ◽  
pp. 37-48 ◽  
Author(s):  
Yoshihiro Hotta ◽  
Hidetsugu Otsuka-Murakami ◽  
Michiko Fujita ◽  
Junichi Nakagawa ◽  
Michio Yajima ◽  
...  

2001 ◽  
Vol 153 (1-2) ◽  
pp. 7-13 ◽  
Author(s):  
Mitsuyoshi Nagura ◽  
Satoshi Iwasaki ◽  
Kunihiro Mizuta ◽  
Hiroyuki Mineta ◽  
Kazuo Umemura ◽  
...  

2004 ◽  
Vol 89 (5) ◽  
pp. 623-628 ◽  
Author(s):  
Blanca Bazán-Perkins ◽  
Mario H. Vargas ◽  
Edgar Sánchez-Guerrero ◽  
Jaime Chávez ◽  
Luis M. Montaño

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