Evidence of 5-HT participation in vagal inhibitory pathway to opossum LES.

1978 ◽  
Vol 234 (3) ◽  
pp. E273 ◽  
Author(s):  
S Rattan ◽  
R K Goyal

Studies were performed in anesthetized opossums to investigate the nature of vagal-stimulated sphincter relaxation, which is resistant to antagonism by a combination of hexamethonium and atropine. The sphincter pressures were measured with water-filled and continuously perfused catheters anchored in the lower esophageal sphincter. Neither increase in the doses of hexamethonium and atropine nor addition of diphenhydramine further modified the vagal response. However, administration of 5-methoxydimethyltryptamine in the presence of hexamethonium and atropine abolished vagally stimulated sphincter relaxation. In animals pretreated with parachlorophenylalanine, addition of atropine and hexamethonium also abolished vagally stimulated sphincter relaxation. In the experiments in which lower esophageal sphincter relaxation on vagal stimulation was abolished, the local stimulation of intramural neurons still produced normal lower esophageal sphincter relaxation. These studies suggest that 5-hydroxytryptamine may participate in the vagal inhibitory pathway to the lower esophageal sphincter.

2003 ◽  
Vol 124 (4) ◽  
pp. A408 ◽  
Author(s):  
Stefania Carmagnola ◽  
Paolo Cantu' ◽  
Daniela Savojardo ◽  
Paolo A. Bianchi ◽  
Roberto Penagini

1992 ◽  
Vol 70 (7) ◽  
pp. 1011-1015 ◽  
Author(s):  
W. G. Paterson ◽  
M. A. B. Anderson ◽  
N. Anand

To characterize the neural pathways involved in lower esophageal sphincter relaxation, intraluminal pressures from the lower esophageal sphincter of the opossum were monitored during swallowing, vagal efferent nerve stimulation, and intraluminal balloon distention in the presence and absence of pharmacologic antagonism of putative neurotransmitters. The combination of atropine, hexamethonium, and 5-methoxydimethyltryptamine, which is known to block ganglionic transmission in the vagal inhibitory pathway to the lower esophageal sphincter, significantly antagonized LES relaxation induced by both swallowing and vagal stimulation, but did not affect the LES relaxation induced by balloon distention. Administration of the nitric oxide synthase inhibitor Nωnitro-L-arginine methyl ester, on the other hand, markedly inhibited LES relaxation induced by vagal stimulation, swallowing, and balloon distention, and this effect was reversed by administration of the nitric oxide synthase substrate L-arginine. These studies indicate that the distension-induced intramural pathway mediating LES relaxation does not involve ganglionic transmission similar to that of the vagal inhibitory pathway to the LES. However, the LES relaxation induced by all forms of stimuli appears to depend on nitric oxide as a final mediator.Key words: ganglionic transmission, muscarinic, nicotinic, serotonergic, nitric oxide.


2009 ◽  
Vol 19 (5) ◽  
pp. 595-600 ◽  
Author(s):  
J. H. Schneider ◽  
M. Küper ◽  
A. Königsrainer ◽  
B. Brücher

2014 ◽  
Vol 51 (2) ◽  
pp. 102-106 ◽  
Author(s):  
Michel Santos PALHETA ◽  
José Ronaldo Vasconcelos da GRAÇA ◽  
Armênio Aguiar dos SANTOS ◽  
Liziane Hermógenes LOPES ◽  
Raimundo Campos PALHETA JÚNIOR ◽  
...  

ContextThe rectal distension in dogs increases the rate of transitory lower esophageal sphincter relaxation considered the main factor causing gastroesophageal reflux.ObjectivesThe aim of this study was evaluate the participation of the nitrergic pathway in the increased transitory lower esophageal sphincter relaxation rate induced by rectal distension in anesthetized dogs.MethodsMale mongrel dogs (n = 21), weighing 10-15 kg, were fasted for 12 hours, with water ad libitum. Thereafter, they were anesthetized (ketamine 10 mg.Kg-1+ xylazine 20 mg.Kg-1), so as to carry out the esophageal motility evaluation protocol during 120 min. After a 30-minute basal period, the animals were randomly intravenous treated whith: saline solution 0.15M (1ml.Kg-1), L-NAME (3 mg.Kg-1), L-NAME (3 mg.Kg-1) + L-Arginine (200 mg.Kg-1), glibenclamide (1 mg.Kg-1) or methylene blue (3 mg.Kg-1). Forty-five min after these pre-treatments, the rectum was distended (rectal distension, 5 mL.Kg-1) or not (control) with a latex balloon, with changes in the esophageal motility recorded over 45 min. Data were analyzed using ANOVA followed by Student Newman-Keuls test.ResultsIn comparison to the respective control group, rectal distension induces an increase in transitory lower esophageal sphincter relaxation. Pre-treatment with L-NAME or methylene blue prevents (P<0.05) this phenomenon, which is reversible by L-Arginine plus L-NAME. However, pretreating with glibenclamide failed to abolish this process.ConclusionsTherefore, these experiments suggested, that rectal distension increases transitory lower esophageal sphincter relaxation in dogs via through nitrergic pathways.


2001 ◽  
Vol 120 (5) ◽  
pp. A632
Author(s):  
Guoxiang Shi ◽  
John E. Pandolfino ◽  
Raymond J. Joehl ◽  
James G. Brassuer ◽  
Peter J. Kahrilas

Sign in / Sign up

Export Citation Format

Share Document