Inhibitory action of ribostamycin sulfate on neuromuscular transmission
Abstract
In common peroneal nerve-anterior tibial muscle preparations of anesthetized cats and isolated rat phrenic nerve-diaphragm preparations, the efficacies of ribosamycin sulfate (RS) blocking neuromuscular transmission were 27% and 72%, respectively in comparison with that of streptomycin sulfate. RS did not affect the resting membrane potential of muscle cells nor the frequency of spontaneous miniature end-plate potential of muscle clls nor the frequency of spontaneous miniature end-plate potential (mepp). However, it prevented the increase by high K+ (30 mmol/L), reduced the amplitude of end-plate potential (epp), and decreased the epp quantal content. The inhibitory action of RS on neuromuscular transmission was antagonized by 4-aminopyridine or CaCl2.
RS inhibited the twitch responses of vasdeferens to field stimulation. The inhibition induced by RS was antagonized by 4-aminopyridine and by increasing the Ca2+ concentration (5 mmol/L) in Mg2+-free Krebs solution, but not antagonized by yohimbine or naloxone. RS also reduced the contractile amplitude of vas deferens induced by norepinephrine or KCl.
It is postulated that the main effect of RS on cholinergic neurotransmission in motor nerve-skeletal muscle junction was to decrease the amount of acetylcholine liberated from nerve endings, whereas the inhibitory effect of RS on adrenergic neurotransmission in vas deferens was mainly by reducing he response of the smooth muscle to endogenous and/or exogenous norepinephrine.
Keywords:
RS inhibited the twitch responses of vasdeferens to field stimulation. The inhibition induced by RS was antagonized by 4-aminopyridine and by increasing the Ca2+ concentration (5 mmol/L) in Mg2+-free Krebs solution, but not antagonized by yohimbine or naloxone. RS also reduced the contractile amplitude of vas deferens induced by norepinephrine or KCl.
It is postulated that the main effect of RS on cholinergic neurotransmission in motor nerve-skeletal muscle junction was to decrease the amount of acetylcholine liberated from nerve endings, whereas the inhibitory effect of RS on adrenergic neurotransmission in vas deferens was mainly by reducing he response of the smooth muscle to endogenous and/or exogenous norepinephrine.