2009
DOI: 10.1007/s12264-009-0624-x
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Nitric oxide inhibits excitatory vagal afferent input to nucleus tractus solitarius neurons in anaesthetized rats

Abstract: Activation of local NO pathway in the NTS could suppress vagal afferent-evoked excitation, suggesting that NO is an important neuromodulator of visceral sensory input in the NTS.

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Cited by 9 publications
(4 citation statements)
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“…By means of double labeling techniques, the absence of colocalization of NOS and TH in cells of the Nsol has been corroborated in amphibians and reptiles (López et al, ; Smeets et al, ). The NO in cells of Nsol has been related with the modulation of visceral sensitive afferents, the control of blood pressure, and the regulation of respiratory frequency (Granjeiro & Machado, ; Kong, Fan, Zhang, Wang, & Wang, ; Lawrence, Castillo‐Meléndez, McLean, & Jarrott, ; Wu et al, ).…”
Section: Discussionmentioning
confidence: 99%
“…By means of double labeling techniques, the absence of colocalization of NOS and TH in cells of the Nsol has been corroborated in amphibians and reptiles (López et al, ; Smeets et al, ). The NO in cells of Nsol has been related with the modulation of visceral sensitive afferents, the control of blood pressure, and the regulation of respiratory frequency (Granjeiro & Machado, ; Kong, Fan, Zhang, Wang, & Wang, ; Lawrence, Castillo‐Meléndez, McLean, & Jarrott, ; Wu et al, ).…”
Section: Discussionmentioning
confidence: 99%
“…The effect of capsaicin was also abrogated by systemic pretreatment with the NO donor SNAP, as was the cardioprotective effect of FNS. Nitric oxide is known to be centrally [30] and peripherally neuroinhibitory and, for example, reduces the activity of non-adrenergic non-cholinergic nerves of the gut [28], modulates afferent nerve activity in the kidney [20], and modulates cardiovascular reflexes via inhibition of cardio-pulmonary C-fiber reflex-induced excitation [15]. We speculated, in our prior study, that release of the circulating cardioprotective factor(s) by rIPC induced by transient limb ischemia and intraarterial adenosine was inhibited by nitric oxide via modulation of peripheral sensory nerve activity [26], and the current data suggest that a similar mechanism might exist with both FNS and capsaicin-mediated release of humoral cardioprotection.…”
Section: Discussionmentioning
confidence: 99%
“…In addition, the absence of colocalization of NOS and TH in cells of the Nsol has been confirmed in amphibians and reptiles López et al, 2005]. Of note, the presence of nitrergic cells in the Nsol led to the suggestion that NO may be related to the modulation of visceral sensitive afferents, the control of blood pressure, and the regulation of respiratory frequency [Lawrence et al, 1998;Wu et al, 2002;Granjeiro and Machado, 2009;Kong et al, 2009].…”
Section: Hindbrainmentioning
confidence: 94%