scholarly journals Neurogenic vasodilatation in isolated bovine and canine penile arteries.

1983 ◽  
Vol 341 (1) ◽  
pp. 603-616 ◽  
Author(s):  
A Bowman ◽  
J S Gillespie
PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e36027 ◽  
Author(s):  
Ana Sánchez ◽  
Cristina Contreras ◽  
María Pilar Martínez ◽  
Belén Climent ◽  
Sara Benedito ◽  
...  

2010 ◽  
Vol 161 (2) ◽  
pp. 350-364 ◽  
Author(s):  
Cristina Contreras ◽  
Ana Sánchez ◽  
Pilar Martínez ◽  
Rafaela Raposo ◽  
Belén Climent ◽  
...  

2014 ◽  
Vol 11 (6) ◽  
pp. 1463-1474 ◽  
Author(s):  
Ana Sánchez ◽  
Cristina Contreras ◽  
Pilar Martínez ◽  
Mercedes Muñoz ◽  
Ana Cristina Martínez ◽  
...  

2016 ◽  
Vol 173 (15) ◽  
pp. 2419-2433 ◽  
Author(s):  
Aisah A Aubdool ◽  
Xenia Kodji ◽  
Nayaab Abdul-Kader ◽  
Richard Heads ◽  
Elizabeth S Fernandes ◽  
...  

2002 ◽  
Vol 39 (4) ◽  
pp. 283-303 ◽  
Author(s):  
Ulf Simonsen ◽  
Albino García-Sacristán ◽  
Dolores Prieto
Keyword(s):  

2000 ◽  
Vol 279 (4) ◽  
pp. H2006-H2012 ◽  
Author(s):  
Kazuhide Ayajiki ◽  
Toshiki Tanaka ◽  
Tomio Okamura ◽  
Noboru Toda

In anesthetized monkeys, electrical stimulation (ES) of the pterygopalatine or geniculate ganglion dilated the ipsilateral ophthalmic artery (OA). The induced vasodilatation was unaffected by phentolamine but potentiated by atropine. Intravenous N G-nitro-l-arginine (l-NNA) abolished the response, which was restored byl-arginine. Hexamethonium-abolished vasodilator responses induced solely by geniculate ganglionic stimulation. Thel-NNA constricted OA; l-arginine reversed the effect. Destruction of the pterygopalatine ganglion constricted the ipsilateral artery. Helical strips of OA isolated under deep anesthesia from monkeys, denuded of endothelium, responded to transmural ES with relaxations, which were abolished by tetrodotoxin and l-NNA but were potentiated by atropine. It is concluded that neurogenic vasodilatation of monkey OA is mediated by nerve-derived nitric oxide (NO), and the nerve is originated from the ipsilateral pterygopalatine ganglion that is innervated by cholinergic neurons from the brain stem via the geniculate ganglion. The OA appears to be dilated by mediation of NO continuously liberated from nerves that receive tonic discharges from the vasomotor center. Acetylcholine liberated from postganglionic cholinergic nerves would impair the release of neurogenic NO.


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