Ketamine inhibits 45Ca influx and catecholamine secretion by inhibiting 22Na influx in cultured bovine adrenal medullary cells

Takara, Hiroshi; Wada, Akihiko; Arita, Masahide; Sumikawa, Koji; Izumi, Fujio

doi:10.1016/0014-2999(86)90030-0

Cited by 20 publications

(8 citation statements)

References 22 publications

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“…Also, studies in this and other laboratories have shown that catecholamine secretion from chromaffin cells evoked by carbachol is markedly more sensitive to anaesthetics than that evoked by direct depolarization. This clearly indicated a direct effect of anaesthetics on the activation of this nicotinic acetylcholine receptor (Takara et al, 1986;Yashima et al, 1986;Pocock & Richards 1987;. This study examines the mechanism of this effect at the ion channel level.…”

Section: Introductdon Methodsmentioning

confidence: 99%

Anaesthetic modulation of nicotinic ion channel kinetics in bovine chromaffin cells

Charlesworth

Richards

1995

British J Pharmacology

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Section: Introductdon Methodsmentioning

confidence: 99%

Anaesthetic modulation of nicotinic ion channel kinetics in bovine chromaffin cells

Charlesworth

Richards

1995

British J Pharmacology

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“…Of the three ion channels in adrenal medullary cells general anaesthetics, such as enflurane (G6thert and Wendt 1977), ketamine (Takara et al 1986), halothane (G6thert et al 1976;Yashima et al 1986) and isoflurane , have been shown to inhibit most strongly the nicotinic acetylcholine receptor-associated ion channels. The order of potency of the inhibitory effect by these anaesthetics is: nicotinic actylcholine receptor-associated ion channels > voltage-dependent Na + channels >> voltage-dependent Ca 2 ÷ channels (Yashima et al 1986;Takara et al 1986.…”

Section: Comparison Of Propofol With Other General Anaesthetics On Iomentioning

confidence: 99%

“…Recently, Lingen et al (1994) have cloned, expressed and pharmacologically characterized the noradrenaline transporter from the bovine adrenal medulla. Since ion channel-mediated catecholamine secretion and antidepressant-sensitive noradrenaline uptake have been well studied in the adrenal medullary cells, this preparation is a good tool for detailed analysis of the action of anaesthetics on the sympathetic nervous system (Sumikawa et al 1980(Sumikawa et al , 1982(Sumikawa et al ,1985Takara et al 1986;Yashima et al 1986;Richards 1988, 1991;Minami et al 1994). …”

Section: Introductionmentioning

confidence: 99%

Inhibitory effects of propofol on catecholamine secretion and uptake in cultured bovine adrenal medullary cells

Minami

Yanagihara

Segawa

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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In the central and peripheral noradrenergic neurons, the balance between noradrenaline release and reuptake determines the level of noradrenaline at the synaptic cleft or the nerve ending. In the present study, we examined the effects of propofol, an intravenous general anaesthetic, on catecholamine secretion and noradrenaline uptake in cultured bovine adrenal medullary cells and on the serum noradrenaline and blood pressure in rats. In cultured adrenal medullary cells, propofol (10-50 mumol/l) concentration-dependently inhibited catecholamine secretion stimulated by carbachol. Propofol suppressed carbachol-evoked 22Na+ influx as well as 45Ca2+ influx at concentrations similar to those which suppressed the catecholamine secretion. Propofol (10-50 mumol/l) also inhibited veratridine-evoked 22Na+ influx, 45Ca2+ influx and catecholamine secretion, whereas it had little effect on the 45Ca2+ influx and catecholamine secretion induced by 56 mmol/l K+. Cultured adrenal medullary cells show [3H] noradrenaline uptake which is sensitive to imipramine. Propofol (10-50 mumol/l) significantly inhibited the imipramine-sensitive uptake of [3H] noradrenaline. In rats, intravenous administration of propofol (2.5 mg/kg) lowered serum noradrenaline and arterial blood pressure. From these findings, in spite of inhibiting noradrenaline uptake, propofol at anaesthetic concentrations (10-30 mumol/l) seems to reduce catecholamine secretion by interfering with Na+ influx through voltage-dependent Na+ channels as well as nicotinic acetylcholine receptor-associated ion channels in the adrenal medulla and, probably, in the sympathetic nervous system. This may explain the propofol-induced hypotension during anaesthesia.

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“…However, one cannot rule out the possibility of ketamine acting at additional neurotransmitter receptors. There are several reports that ketamine can block the ion channel of the nicotinic acetylcholine receptor (Aronstam et al, 1982;Takara et al, 1986), interact with the sigma-opioid receptors (Parsons et al, 1981) and can affect the dopaminergic system (Rao et al, 1989).…”

Section: Fig 5 Characterisation Of the Ketamine-mediated Inhibitionmentioning

confidence: 99%

Ketamine-Mediated Inhibition of Rabies Virus Infection in vitro and in Rat Brain

Lockhart

Tsiang

Ceccaldi

et al. 1991

Antivir Chem Chemother

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SummaryThis report describes the effect of the dissociative anaesthetic ketamine, a non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, on the infectivity of the neurotropic rabies virus, in neuronal culture systems and in vivo. produced an approximate 10Q-1000-fold decrease in the production of rabies virus in neuronal cell cultures. Rabies virus infection was also inhibited in non-neuronal cell lines (Baby Hamster Kidney fibroblasts) but the inhibitory effects appeared better expressed in cells of neuronal origin (neuroblastoma and primary neuronal cultures). The kalnate/quisqualate competitive antagonist CNQX did not modify the course of rabies virus infection and modulators of known NMDA regulatory sites (Mg 2 + , Zn 2 + , HA-966) failed to antagonize the ketamine-rnediated inhibition of rabies virus production in neuroblastoma cells. Furthermore, Ca 2 +-mobilization does not appear to be involved because Ca 2 +-depleted and EGTA-treated medium did not affect the normal production of rabies virus. The action of ketamine on rabies virus infection in vivo was also investigated; peripheral treatment ofrats with this drug inhibited rabies virus infection in the thalamus, cortex and hippocampal formation (in particular the pyramidal layer of the CA1 region). Taken together, these data suggest that the ketamine-mediated inhibition of rabies virus production in vitro, although highly selective, is not acting via classic NMDA receptor-mediated mechanisms. However, the ketaminemediated retardation of rabies virus infection in vivo may offer new prospects for post-exposure rabies antiviral therapy.

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Ketamine inhibits 45Ca influx and catecholamine secretion by inhibiting 22Na influx in cultured bovine adrenal medullary cells

Cited by 20 publications

References 22 publications

Anaesthetic modulation of nicotinic ion channel kinetics in bovine chromaffin cells

Anaesthetic modulation of nicotinic ion channel kinetics in bovine chromaffin cells

Inhibitory effects of propofol on catecholamine secretion and uptake in cultured bovine adrenal medullary cells

Ketamine-Mediated Inhibition of Rabies Virus Infection in vitro and in Rat Brain

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