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Pregled bibliografske jedinice broj: 727026

The mechanism of alpha2-adrenergic inhibition of sympathetic ganglionic transmission


McCallum, ruce J.; Boban, Nataša; Hogan, Quinn; Schmeling, William T.; Kampine, John P.; Bošnjak, Željko J.
The mechanism of alpha2-adrenergic inhibition of sympathetic ganglionic transmission // Anesthesia and analgesia, 87 (1998), 3; 503-510 doi:10.1213/00000539-199809000-00001 (međunarodna recenzija, članak, znanstveni)


Naslov
The mechanism of alpha2-adrenergic inhibition of sympathetic ganglionic transmission

Autori
McCallum, ruce J. ; Boban, Nataša ; Hogan, Quinn ; Schmeling, William T. ; Kampine, John P. ; Bošnjak, Željko J.

Izvornik
Anesthesia and analgesia (0003-2999) 87 (1998), 3; 503-510

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
Acetylcholine/metabolism; Action Potentials/drug effects; Adrenergic alpha-2 Receptor Antagonists*; Ganglia; Sympathetic/drug effects*; Imidazoles/pharmacology*; Medetomidine; Norepinephrine/pharmacology; Stellate Ganglion/drug effects; Synaptic Transmission/drug effects*

Sažetak
Abstract Alpha2-adrenergic agonists produce analgesia and reduce hemodynamic stress through central and peripheral mechanisms, but the effect of adrenergic agonists on pre- and postganglionic sites has not yet been clarified. In this study, we examined the effects of dexmedetomidine (DMT), an alpha2-agonist, on neural conduction and neurotransmitter release in sympathetic ganglia. The stellate ganglia from 48 mongrel dogs were isolated, desheathed, and superfused with Krebs' solution. Compound action potentials were evoked, and chromatography was used to detect acetylcholine released by preganglionic stimulation in the presence or absence of DMT. To further elucidate the mechanism of alpha2 effects, DMT was applied in combination with the alpha2-antagonist atipamezole (AT) or the imidazoline antagonist idazoxan (ID). In other experiments, DMT was applied in the presence of exogenous nicotinic stimulation with 1, 1-dimethyl-4-phenylpiperazinium iodide or muscarinic stimulation with (+)cis-dioxolane. DMT dose-dependently inhibited synaptic transmission with a 50% effective dose of 71.6 (26.0-174.3) microM. Neurotransmitter release was reduced 25% by 70 microM DMT during low-frequency (0.4 Hz) stimulation, but this effect was abolished at higher frequency (5 Hz) stimulation. AT but not ID blocked the inhibitory action of DMT. DMT inhibited the excitatory postsynaptic response to exogenous muscarinic stimulation but not nicotinic stimulation. These results indicate that alpha2-receptor activation depresses ganglionic transmission through postsynaptic inhibition of muscarinic stimulation, although reduction of neurotransmitter release through a presynaptic autofeedback mechanism is also involved.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Javno zdravstvo i zdravstvena zaštita



POVEZANOST RADA


Autor s matičnim brojem:
Nataša Boban, (246494)

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE


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