Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Differential effects of general anesthetics on G protein-coupled inwardly rectifying and other potassium channels
Autore:
Yamakura, T; Lewohl, JM; Harris, A;
Indirizzi:
Univ Texas, Inst Mol & Cellular Biol, Austin, TX 78712 USA Univ Texas Austin TX USA 78712 Mol & Cellular Biol, Austin, TX 78712 USA Waggoner Ctr Alcohol & Addict Res, Neurobiol Sect, Austin, TX USA WaggonerCtr Alcohol & Addict Res Austin TX USA iol Sect, Austin, TX USA
Titolo Testata:
ANESTHESIOLOGY
fascicolo: 1, volume: 95, anno: 2001,
pagine: 144 - 153
SICI:
0003-3022(200107)95:1<144:DEOGAO>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
SITE-DIRECTED MUTAGENESIS; MU-OPIOID RECEPTOR; GATED ION CHANNELS; K+-CHANNEL; MOLECULAR-BASIS; VOLATILE ANESTHETICS; CARDIAC-ARRHYTHMIA; MESSENGER-RNAS; RAT-BRAIN; CLONING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Harris, A Univ Texas, Inst Mol & Cellular Biol, 2500 Speedway MBB 1-124, Austin, TX 78712 USA Univ Texas 2500 Speedway MBB 1-124 Austin TX USA 78712 78712 USA
Citazione:
T. Yamakura et al., "Differential effects of general anesthetics on G protein-coupled inwardly rectifying and other potassium channels", ANESTHESIOL, 95(1), 2001, pp. 144-153

Abstract

Background General anesthetics differentially affect various families of potassium channels, and some potassium channels are suggested to be potential targets for anesthetics and alcohols. Methods: The voltage-gated (ERG1, ELK1, and KCNQ2/3) and Inwardly rectifying (GIRK1/2, GIRK1/4, GIRK2, IRK1, and ROMK1) potassium channels were expressed in Xenopus oocytes. Effects of volatile agents [halothane, isoflurane,enflurane, F3 (1-chloro-1,2,2-trifluorocyclobutane), and the structurally related nonimmobilizer F6 (1,2-dichlorohexafluorocyclobutane)], as well as intravenous (pentobarbital propofol, etomidate, alphaxalone, ketamine), andgaseous (nitrous oxide) anesthetics and alcohols (ethanol and hexanol) on channel function were studied using a two-electrode voltage clamp. Results: ERG1, ELK1, and KCNQ2/3 channels were either inhibited slightly or unaffected by concentrations corresponding to twice the minimum alveolar concentrations or twice the anesthetic EC,, of volatile and intravenous anesthetics and alcohols. In contrast, G protein-coupled inwardly rectifying potassium (GIRK) channels were inhibited by volatile anesthetics but not by intravenous anesthetics. The neuronal-type GIRK1/2 channels were inhibited by 2 minimum alveolar concentrations of halothane or F3 by 45 and 81%, respectively, whereas the cardiac-type GIRK1/4 channels were inhibited only by F3. Conversely, IRK1 and ROMK1 channels were completely resistant to all anesthetics tested. Current responses of GIRK2 channels activated by mu -opioid receptors were also inhibited by halothane. Nitrous oxide (similar to0.6atmosphere) slightly but selectively potentiated GIRK channels. Results ofchimeric and multiple amino acid mutations suggest that the region containing the transmembrane domains, but not the pore-forming domain, may be Involved in determining differences in anesthetic sensitivity between GIRK and IRK channels. Conclusions: G protein-coupled inwardly rectifying potassium channels, especially those composed of GIRK2 subunits, were inhibited by clinical concentrations of volatile anesthetics. This action may be related to some side effects of these agents.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 15:20:36