Ganglionic Inhibition by Dopamine and Neurogenic Vasodilatation

2015 ◽  
pp. 241-247 ◽  
Author(s):  
J. L. Willems ◽  
M. G. Bogaert
Keyword(s):  
Neurogenic Vasodilatation

scholarly journals TRPA1 activation leads to neurogenic vasodilatation: involvement of reactive oxygen nitrogen species in addition to CGRP and NO

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

Evidence for nitroxidergic innervation in monkey ophthalmic arteries in vivo and in vitro

2000 ◽  
Vol 279 (4) ◽  
pp. H2006-H2012 ◽  
Author(s):  
Kazuhide Ayajiki ◽  
Toshiki Tanaka ◽  
Tomio Okamura ◽  
Noboru Toda
Keyword(s):  
Ophthalmic Artery ◽  
Cholinergic Neurons ◽  
Geniculate Ganglion ◽  
Cholinergic Nerves ◽  
Neurogenic Vasodilatation ◽  
Pterygopalatine Ganglion ◽  
The Brain ◽  
Ophthalmic Arteries

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.

Diverse interactions of calcitonin gene related peptide and nitric oxide in the gastric and cutaneous microcirculation

1995 ◽  
Vol 73 (7) ◽  
pp. 991-994 ◽  
Author(s):  
P. Holzer ◽  
Ch. Wachter ◽  
M. Jocič ◽  
I. Th. Lippe ◽  
A. Heinemann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Mucosa ◽  
Calcitonin Gene Related Peptide ◽  
Afferent Nerve ◽  
Nerve Fibres ◽  
Related Peptide ◽  
Neurogenic Vasodilatation ◽  
Cutaneous Microcirculation ◽  
Cgrp Release ◽  
Calcitonin Gene

Calcitonin gene related peptide (CGRP) is the major mediator of afferent nerve mediated vasodilatation in the gastric mucosa and skin of the rat. Since receptors for CGRP occur on both the vascular endothelium and smooth muscle, it is conceivable that the vascular actions of CGRP involve multiple mechanisms. The vasodilator effect of rat CGRP-α in the rat gastric mucosa is indeed inhibited by blockade of nitric oxide (NO) synthesis, as is the gastric mucosal hyperemia in response to gastric acid challenge, which is mediated by CGRP release from afferent nerve fibres. In contrast, the vasodilator response to rat CGRP-α in the rat hind paw and the CGRP-mediated vasodilatation evoked by antidromic stimulation of afferent nerve fibres do not depend on the formation of NO. These data indicate that NO plays regionally different roles in the local vasodilator action of CGRP. NO is a secondary vasorelaxant messenger of CGRP in the gastric, but not in the cutaneous, microcirculation. However, this L-arginine-derived autacoid may have a role in the irritant-induced CGRP release from afferent vasodilator fibres in the skin.Key words: calcitonin gene related peptide, nitric oxide, microcirculation, gastric mucosa, skin, afferent nerve fibres, neurogenic vasodilatation.

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