Adrenaline inhibits muscarinic transmission in bullfrog sympathetic ganglia

Akasu, Takashi

doi:10.1007/bf00581811

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…So far, these do not include ATP, muscarine and LHRH, all of which blocked IM. Isoproterenol (3 /tM) was without effect on IH (n = 4), which also blocks IM (Akasu, 1988(Akasu, , 1989.…”

Section: Involvement Ofprotein Kinase a In Ih Regulationmentioning

confidence: 99%

Cyclic AMP regulates an inward rectifying sodium‐potassium current in dissociated bull‐frog sympathetic neurones.

Tokimasa

Akasu

1990

The Journal of Physiology

115

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SUMMARY1. Bull-frog sympathetic neurones in primary culture were voltage clamped in the whole-cell configuration. The pipette solution contained ATP (5 mM).2. A hyperpolarization-activated sodium-potassium current (H-current: IH) was separated from other membrane currents in a nominally calcium-free solution containing cobalt (2 mM), magnesium (4 mM), barium (2 mm), tetraethylammonium (20 mM), tetrodotoxin (3 /,M), apamin (30 nM) and 4-aminopyridine (1 mm). IH was selectively blocked by caesium (10-300 ,UM).3. The steady-state activation Of IH occurred between -60 and -130 mV. The H-conductance was 4-1-6-6 nS at the half-activation voltage of -90 mV. With the concentrations of potassium and sodium ions in the superfusate at 20 and 70 mm, respectively, the reversal potential of IH was about -20 mV. IH was activated with a time constant of 2-8 s at -90 mV and 22 'C. The Q10 between 16 and 26 'C was 4-3. 4. A non-hydrolysable ATP analogue in the pipette solution did not support IH activation. Intracellular 'loading' of GTP-y-S (30-500,M) led to a progressive activation of IH-5. Forskolin (10 ,UM) increased the maximum conductance ofIH by 70 %. This was associated with a depolarizing shift in the half-activation voltage (5-10 mV) and in the voltage dependence of the activation/deactivation time constant ofIH.6. Essentially the same results as with forskolin were obtained by intracellular 'loading' with cyclic AMP (3-10 /LM) or bath application of 8-bromo cyclic AMP (0-1-1 mM), dibutyryl cyclic AMP (1 mM) and 3-isobutyl-1-methylxanthine

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“…So far, these do not include ATP, muscarine and LHRH, all of which blocked IM. Isoproterenol (3 /tM) was without effect on IH (n = 4), which also blocks IM (Akasu, 1988(Akasu, , 1989.…”

Section: Involvement Ofprotein Kinase a In Ih Regulationmentioning

confidence: 99%

Cyclic AMP regulates an inward rectifying sodium‐potassium current in dissociated bull‐frog sympathetic neurones.

Tokimasa

Akasu

1990

The Journal of Physiology

115

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“…It also reduces the amplitude of slow postsynaptic currents induced by acetylcholine. In bullfrogs the inhibition of muscarinic transmission induced by noradrenaline is reported to be due to direct suppression of the muscarinic current at the postsynaptic membrane of sympathetic ganglia [19]. So the antagonised b-adrenergic effects induced by esmolol may cause the enhancement of potential amplitude of acetylcholine during neuromuscular transmission.…”

Section: Discussionmentioning

confidence: 99%

Neuromuscular interactions between mivacurium and esmolol in rabbits

Kim

Shin

et al. 1998

Anaesthesia

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SummaryWe compared the dose-response relationship and the neuromuscular blocking effects of mivacurium during infusions of esmolol in 40 anaesthetised rabbits. Train-of-four stimuli were applied every 10 s to the common peroneal nerve and the force of contraction of the tibialis anterior muscle was measured. Plasma cholinesterase activity decreased by 13% after esmolol infusion. .min ¹1, respectively (p < 0.001). The duration of neuromuscular block with mivacurium 0.16 mg.kg ¹1 was prolonged by 30% with esmolol due to diminished plasma cholinesterase activity (p < 0.05). Heart rate and mean arterial blood pressure decreased by 15% with esmolol (p < 0.05). The results of this study show that, in rabbits, esmolol decreased plasma cholinesterase activity, antagonised the neuromuscular blocking potency of mivacurium and prolonged its neuromuscular blocking effect. Esmolol is a water-soluble, cardioselective b-adrenoceptor antagonist with a rapid onset and ultrashort duration of action due to its short elimination half-life of 9 min [1]. As an ester it is rapidly metabolised by esterases in the blood to a free acid metabolite which has a b-adrenergic blocking potency 1/1600 that of the parent drug. The hydrolysis reaction occurs mainly in the cytosol of red blood cells but not in plasma [2]. Esmolol is widely used as a treatment for various cardiovascular diseases, including supraventricular tachyarrhythmias, hypertension and angina pectoris [3].Mivacurium is a nondepolarising muscle relaxant which has recently been introduced into clinical practice. Although chemically related to atracurium, it has a shorter duration of action [4,5]. It is hydrolysed by plasma cholinesterase in vitro at 70-88% the rate of suxamethonium [6][7][8]. Esmolol is reported to inhibit human plasma cholinesterase activity by 50% in vitro [9]. There are no 'in vivo' reports of pharmacological interactions between esmolol and mivacurium. The present study was undertaken to compare the dose-response relationships and the neuromuscular blocking effects of mivacurium during infusions of esmolol in anaesthetised rabbits. Method

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Synaptic transmission and function of parasympathetic ganglia

Akasu

Nishimura

1995

Progress in Neurobiology

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Adrenaline inhibits muscarinic transmission in bullfrog sympathetic ganglia

Cited by 4 publications

References 32 publications

Cyclic AMP regulates an inward rectifying sodium‐potassium current in dissociated bull‐frog sympathetic neurones.

Cyclic AMP regulates an inward rectifying sodium‐potassium current in dissociated bull‐frog sympathetic neurones.

Neuromuscular interactions between mivacurium and esmolol in rabbits

Synaptic transmission and function of parasympathetic ganglia

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