Disruption of muscarinic receptor-G protein coupling is a general property of liquid volatile anesthetics
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Cited by (53)
Inhalation anaesthetic isoflurane inhibits the muscarinic cation current and carbachol-induced gastrointestinal smooth muscle contractions
2018, European Journal of PharmacologyCitation Excerpt :In contrast, inhibition of muscarinic receptors, G-proteins or their coupling by isoflurane seems a much more likely underlying mechanism of mICAT suppression. This is not only consistent with several previous studies showing that isoflurane can inhibit muscarinic receptors (Minami et al., 1994; Do et al., 2001) and disrupt muscarinic receptor - G protein coupling (Anthony et al., 1989; Magyar and Szabo, 1996; Hollmann et al., 2005), but also has direct experimental support. Indeed, mICAT was not simply “scaled” down by isoflurane, as would be expected in case of simple channel block, but instead its biophysical properties were altered - specifically, the potential of half-maximal activation shifted positively while voltage-dependent deactivation kinetics was accelerated (Figs. 1 and 2).
Effects of isoflurane on prefrontal acetylcholine release and hypothalamic Fos response in young adult and aged rats
2004, Experimental NeurologyCitation Excerpt :Previous in vitro experiments indicate that isoflurane increases intracellular calcium concentrations (Iaizzo, 1992; Kindler et al., 1999), which may decrease agonist responses. Isoflurane may interfere with muscarinic ACh receptor-mediated signaling, possibly in a G-protein-dependent way (Anthony et al., 1989; Forman et al., 1995; Nietgen et al., 1998). Recent studies suggest that the neuronal nicotinic receptor may be the main target mediating isoflurane anesthesia (Flood et al., 1997; Puil and el-Beheiry, 1990; Salord et al., 1997).
Cholinergic mechanisms mediating anesthetic induced altered states of consciousness
2004, Progress in Brain ResearchCitation Excerpt :Volatile drugs including chloroform, enflurane and isoflurane increase muscarinic antagonist binding by decreasing the ligand-receptor dissociation rate. These drugs also interfere with the muscarinic receptor–G protein interaction (Dennison et al., 1987; Anthony et al., 1988, 1989). Halothane and enflurane inhibit m1 receptor signalling (Lin et al., 1993; Durieux, 1995), and while this receptor subtype does not appear to be inhibited by isoflurane, m3 signalling has been shown to be affected (Nietgen et al., 1998; Do et al., 2001).
Role of ryanodine receptors in chloroform-induced contraction in swine tracheal smooth muscle
2002, Toxicology and Applied PharmacologyAnaesthetic actions on other targetes: Protein kinase C and guanine nucleotide-binding proteins
2002, British Journal of AnaesthesiaCitation Excerpt :Similarly, halothane affects oxotremorine binding in rat brainstem membranes.32 Persistence of this high-affinity receptor state is also found with other volatile agents like chloroform, enflurane, isoflurane and diethylether.3 Volatile anaesthetics also cause a rightwards shift in the dose of clonidine, a partial α2-agonist, to inhibit adenylyl cyclase (AC).