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Modulation by nitric oxide (NO) of the intensity of non-quantum mediator secretion in neuromuscular junctions in rats
Experiments on rat diaphragm muscle showed that the nitric oxide (NO) donors sodium nitroprusside SNP) and S-nitroso-N-acetylpenicillamine (SNAP). as well as L-arginine. a substrate for NO synthesis. decreased the level of muscle fiber hyperpolarization (the H effect) after blockade of cholinoceptor...
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Published in: | Neuroscience and behavioral physiology 2001-07, Vol.31 (4), p.451-455 |
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creator | Mukhtarov, M R Urazaev, A K Nikolskii, E E Vyskocil, F |
description | Experiments on rat diaphragm muscle showed that the nitric oxide (NO) donors sodium nitroprusside SNP) and S-nitroso-N-acetylpenicillamine (SNAP). as well as L-arginine. a substrate for NO synthesis. decreased the level of muscle fiber hyperpolarization (the H effect) after blockade of cholinoceptors on the postsynaptic membrane by d-tubocurarine in conditions of irreversible inhibition of acetylcholinesterase with armine. Conversely, disruptions to NO synthesis in muscle fibers by the NO synthase blocker NG-nitro-L-arginine methyl ester (L-NAME) led to increases in the H effect both in vitro and in vivo. Inactivated solutions of sodium nitroprusside and inactive forms of arginine and NAME (D-arginine. D-NAME) had no effect on the magnitude of the H effect, while hemoglobin, which efficiently binds NO molecules, blocked the inhibitory effects of sodium nitroprusside. SNAP, and L-arginine on the magnitude of the H effect. All these points provide evidence that NO can function as a modulator of non-quantum mediator release in the neuromuscular junctions of warm-blooded animals. |
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Conversely, disruptions to NO synthesis in muscle fibers by the NO synthase blocker NG-nitro-L-arginine methyl ester (L-NAME) led to increases in the H effect both in vitro and in vivo. Inactivated solutions of sodium nitroprusside and inactive forms of arginine and NAME (D-arginine. D-NAME) had no effect on the magnitude of the H effect, while hemoglobin, which efficiently binds NO molecules, blocked the inhibitory effects of sodium nitroprusside. SNAP, and L-arginine on the magnitude of the H effect. 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Conversely, disruptions to NO synthesis in muscle fibers by the NO synthase blocker NG-nitro-L-arginine methyl ester (L-NAME) led to increases in the H effect both in vitro and in vivo. Inactivated solutions of sodium nitroprusside and inactive forms of arginine and NAME (D-arginine. D-NAME) had no effect on the magnitude of the H effect, while hemoglobin, which efficiently binds NO molecules, blocked the inhibitory effects of sodium nitroprusside. SNAP, and L-arginine on the magnitude of the H effect. 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subjects | Acetylcholine - metabolism Animals Enzyme Inhibitors - pharmacology Excitatory Postsynaptic Potentials - drug effects Extracellular Space - physiology In Vitro Techniques Membrane Potentials - drug effects Motor Neurons - physiology Muscle, Skeletal - innervation Muscle, Skeletal - physiology Nerve Endings - physiology Neuromuscular Junction - metabolism Neuromuscular Junction - physiology Neurotransmitter Agents - metabolism Neurotransmitter Agents - physiology NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - biosynthesis Nitric Oxide - physiology Nitric Oxide Donors - pharmacology Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase Type III Rats Synapses - drug effects Synapses - physiology |
title | Modulation by nitric oxide (NO) of the intensity of non-quantum mediator secretion in neuromuscular junctions in rats |
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