The pharmacology of the efferent function of sensory nerves.

Maggi, Carlo Alberto

doi:10.1111/j.1474-8673.1991.tb00317.x

Cited by 180 publications

(77 citation statements)

References 224 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This would explain the resistance of these relaxations to ganglionic blockade as well as their sensitivity to capsaicin pretreatment. Capsaicin is a neurotoxin relatively selective for small afferent fibres (see Maggi, 1991). Indeed, our capsaicin protocol did not inhibit the cholinergic contractions or the adrenergic relaxations of our preparation and only marginally inhibited the non-adrenergic relaxations elicited by stimulation of the preganglionic parasympathetic fibres carried by the recurrent laryngeal nerves.…”

Section: Capsaicin-sensitive Relaxant Innervationmentioning

confidence: 99%

Relaxant innervation of the guinea‐pig trachealis: demonstration of capsaicin‐sensitive and ‐insensitive vagal pathways.

Canning

Undem

1993

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. The guinea-pig trachea was isolated with its extrinsic innervation intact and placed in a water-jacketed dissecting dish containing warmed, oxygenated Krebs solution. The trachea was not separated from the oesophagus. Two adjacent cartilage rings of the rostral portion of the trachea were cut open opposite the trachealis and prepared for isometric tension measurements.2. Following the addition of atropine and contraction of the trachealis with prostaglandin F2a (PGF2.), stimulation of the cervical sympathetic trunks elicited relaxations that were abolished by propranolol or hexamethonium. Stimulation of the vagus nerves caudal to the nodose ganglia also elicited relaxations. These vagally mediated relaxations were unaffected by propranolol but were abolished by hexamethonium or by cutting the recurrent laryngeal nerves. 3. After cutting the vagi caudal to the nodose ganglia, stimulation of the vagi rostral to the nodose ganglia elicited relaxations of the trachealis that were not significantly affected by either propranolol or hexamethonium but were abolished by cutting the superior laryngeal nerves. Stimulation of right vagi which had undergone supranodose vagotomy 14 days prior to experimentation was without effect on the smooth muscle of the guinea-pig trachea while the response to stimulation of the left vagus was unchanged.4. Acute capsaicin desensitization abolished relaxations of the guinea-pig trachealis elicited by stimulation of the vagal fibres carried by the superior laryngeal nerves. In contrast, capsaicin desensitization only modestly inhibited relaxations elicited by stimulation of the preganglionic parasympathetic fibres carried by the recurrent laryngeal nerves and had no effect on sympathetic nerve-induced relaxations.5. Removing the oesophagus selectively abolished relaxations elicited by stimulation of both vagal pathways of non-adrenergic relaxant innervation. Nonadrenergic relaxations of the trachealis elicited by electrical field stimulation were unaffected by removing the oesophagus. Oesophagus removal also had no effect on the parasympathetic-cholinergic contractile innervation or the sympathetic relaxant innervation of the trachealis.* To whom correspondence should be addressed. MS 1153B. J. CANVING AND B. J. UTNDEM 6. The results indicate that the guinea-pig trachealis receives non-adrenergic relaxant innervation from both parasympathetic and capsaicin-sensitive vagal pathways. The results also suggest that the neurones mediating non-adrenergic relaxations of the trachea are sensitive to oesophagus removal. The observation that oesophagus removal abolishes parasympathetic relaxations of the trachealis while having no effect on parasympathetic contractions supports the hypothesis that the guinea-pig trachealis receives excitatory and inhibitory innervation from distinct vagal parasympathetic pathways.

show abstract

Section: Capsaicin-sensitive Relaxant Innervationmentioning

confidence: 99%

Relaxant innervation of the guinea‐pig trachealis: demonstration of capsaicin‐sensitive and ‐insensitive vagal pathways.

Canning

Undem

1993

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…In the periphery, it is the predominant neurotransmitter found in nociceptive nerves. The release of substance P, and other neuropeptides, from sensory nerves is thought to play a significant role in the neural component of inflammation (i.e., neurogenic inflammation), 123 which encompasses increased vascular permeability and vasodilation. Indeed, it was found that mice that lack the receptor for substance P (tachykinin NK 1 receptor) fail to exhibit normal inflammatory responses.…”

Section: Kinin Antagonistsmentioning

confidence: 99%

Multifunctional Drugs for Head Injury

2009

View full text Add to dashboard Cite

Summary: Traumatic brain injury (TBI) remains one of the leading causes of mortality and morbidity worldwide in individuals under the age of 45 years, and, despite extensive efforts to develop neuroprotective therapies, there has been no successful outcome in any trial of neuroprotection to date. In addition to recognizing that many TBI clinical trials have not been optimally designed to detect potential efficacy, the failures can be attributed largely to the fact that most of the therapies investigated have been targeted toward an individual injury factor. The contemporary view of TBI is that of a very heterogenous type of injury, one that varies widely in etiology, clinical presentation, severity, and pathophysiology. The mechanisms involved in neuronal cell death after TBI involve an interaction of acute and delayed anatomic, molecular, biochemical, and physiological events that are both complex and multifaceted. Accordingly, neuropharmacotherapies need to be targeted at the multiple injury factors that contribute to the secondary injury cascade, and, in so doing, maximize the likelihood of a successful outcome. This review focuses on a number of such multifunctional compounds that have shown considerable success in experimental studies and that show maximum promise for success in clinical trials.

show abstract

“…The finding that the sensory afferent system may also have an "efferent" function has been a fundamental step in the appreciation of the mechanisms involved in neurogenic inflammation (17). Furthermore, the peripheral endings of the primary afferent sensory neurons not only transmit nociceptive stimuli, but also induce vasodilation, increase venular permeability, modify the activity of the immune sys- Widespread changes in the neural network in SSc, characterized by a uniform and dynamic neuronal degeneration in the affected and nonaffected skin, are reported (26,27).…”

mentioning

confidence: 99%