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PubMed1977

Evidence for a nicotinic receptor in the sinus node.

The sinus node of the guinea pig was perfused in vitro and potassium uptake was studied in the absence and in the presence of several nicotinic agonists and antagonists. The following results were obtained: (1) the decrease in K uptake caused by a low (10(-9)M) concentration of acetylcholine was changed to an increase when acetylcholine was given in the presence of nicotinic blockade; (2) a small concentration (10(-10)M) of atropine potentiated the decrease in K uptake induced by a low concentration of acetylcholine and 10(-8)M atropine abolished it: (3) a small concentration of nicotine (10(-10)M) decreased K uptake; (4) 1,1-dimethyl-4-phenylpiperazinium (DMPP) did not modify K uptake; (5) the lack of effect of DMPP was not affected by hexamethonium; (6) trimethylphenylammonium (TMPA) decreased K uptake; and (7) the inhibitory effect of TMPA was abolished by decamethonium. It is concluded that a nicotinic receptor in the sinus node mediates the inhibitory action of a low concentration of acetylcholine on K uptake.

Acetylcholine↗
PubMed1995

Alkylating derivative of hexadecamethonium protects muscle synaptic acetylcholinesterase against inhibition.

The action of the alkylating derivative of hexadecamethonium on frog neuromuscular transmission was studied with the help of intracellular microelectrodes. Treatment of frog m. cutaneous pectoris-n. pectoralis preparations with the alkylating derivative of hexadecamethonium (0.5 microM) for 30 min led to an irreversible decrease in the amplitude of the end-plate potentials by 2.5-fold without a change of their latency period or quantal content. Such treatment led also to a considerable reduction of the anticholinesterase effects of neostigmine and of the organophosphorus irreversible inhibitor, armine. Thus, when applied to intact nerve-muscle preparations, neostigmine (2 microM) or armine (1 microM) increased the amplitude of end-plate potentials by 80-90%, and the rise time and half-decay time by about 2- to 3-fold. However, after the nerve-muscle preparations were pretreated with the alkylating derivative of hexadecamethonium (0.5 microM, for 30 min), the amplitude of end-plate potentials increased by 20-25%, rise time by 15-20% and half-decay time by 40-50% only. Investigation of muscle acetylcholinesterase activity, using the Ellman technique, showed that the alkylating derivative of hexadecamethonium diminished the sensitivity of the muscle acetylcholinesterase to inhibition without exerting its own inhibitory action.

Action Potentials↗
PubMed1996

Capillary electrophoresis analysis of chemical warfare agent breakdown products. I. Counterelectroosmotic separation of alkylphosphonic acids and their monoester derivatives.

An analytical method has been developed for the analysis of chemical warfare agents by capillary zone electrophoresis (CZE). Sorbate anion has been selected as indirect UV-absorbing agent and decamethonium cation reduces the electroosmotic flow. The optimized electrolyte (5 mM sorbic acid, 0.1 mM decamethonium bromide pH 6) allows the simultaneous separation of alkylphosphonic acids and their monoester derivatives in less than 15 min. The measurement of phosphonic solutes has been achieved in spiked soils using calibration curves in the 5-50 mg/l concentration range.

Alkylation↗
PubMed1983

Neuromuscular blocking properties of suxamethonium and decamethonium in normal and myasthenic rat muscle.

Patients with myasthenia gravis (MG) have increased tolerance to the neuromuscular blocking properties of suxamethonium (SCh) and decamethonium (C10) and exhibit a reversal of the C10-induced block by neostigmine. The effects of these drugs were compared in forelimb flexor digitorum longus muscle from normal rats and from rats with experimental autoimmune myasthenia gravis (EAMG) to investigate the similarity of EAMG to MG. The depolarization induced by 1, 5, 10 and 25 microM SCh or C10 at the motor end-plates was significantly higher in normal than in EAMG muscle. However, both normal and EAMG end-plates responded in a similar qualitative manner to each drug. The depolarization produced by SCh was typically maintained until the drug was washed from the bath. The depolarization produced by C10 tended to decrease after reaching its peak despite continued application of the drug. With both drugs, miniature end-plate potential (MEPP) amplitude reduction is maintained until a saline wash. Neostigmine interaction with SCh and C10 in normal and EAMG muscle was compared by measuring isometric twitch tension in vitro. Neostigmine potentiated the neuromuscular block produced by either SCh or C10 in both normal and EAMG muscle. Thus muscle from rats with EAMG shares with MG an increased tolerance to SCh and C10 when compared to normal muscle but does not exhibit the qualitatively different interaction of C10 affected muscle with neostigmine that is found in MG patients. This and other studies comparing EAMG and MG indicate that EAMG is an appropriate model of MG but differences such as we have noted should be considered when extrapolating data from EAMG to the human disease.

Animals↗