The effect of procaine on neuromuscular transmission

Kordaš, M.

doi:10.1113/jphysiol.1970.sp009186

Cited by 83 publications

(42 citation statements)

References 15 publications

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“…As a consequence it raises the electrical threshold and suppresses the ionic conductance of the membrane (Narahashi, Frazier & Yamada, 1970;Narahashi, Frazier & Takano, 1976). Furthermore, procaine does not modify the quantal release from the nerve terminal but prolongs the activation of the Na-channel by acetylcholine (Furukawa, 1957;Maeno, 1966;Steinbach, 1968;Gage & Armstrong, 1968;Kordas, 1970;Deguchi & Narahashi, 1971).…”

Section: Discussionmentioning

confidence: 99%

Actions of 4‐aminopyridine on Vascular Smooth Muscle Tissues of the Guinea‐pig

Hara

Kitamura

Kuriyama

1980

British J Pharmacology

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I Effects of 4-aminopyridine (4-AP) and procaine on the membrane and contractile properties of smooth muscle cells of the guinea-pig pulmonary artery and portal vein were observed. 2 The membrane potential and length constant of smooth muscle cells of the guinea-pig pulmonary artery were -53.2 mV and 1.2 mm, respectively, and those of the portal vein were -52.6 mV and 0.71 mm, respectively. The membrane was electrically quiescent in the pulmonary artery and it was electrically active in the portal vein. 3 Both 4-AP and procaine depolarized the membrane, increased the membrane resistance and suppressed the rectifying properties in both tissues. Both agents evoked a graded response from the muscle membranes of the pulmonary artery by outward current pulse. Procaine had a greater effect than 4-AP on the above membrane properties. The results suggest that 4-AP and procaine suppress K-conductance of the muscle membrane, and 4-AP but not procaine increases noradrenaline release from the nerve terminal. Presumably intracellular free Ca concentrations are also modified by these agents. The effects of 4-AP and procaine on the vascular muscle were compared with those on other excitable tissues.

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Section: Discussionmentioning

confidence: 99%

Actions of 4‐aminopyridine on Vascular Smooth Muscle Tissues of the Guinea‐pig

Hara

Kitamura

Kuriyama

1980

British J Pharmacology

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“…During exposure to procaine at pH 7-4 at the resting membrane potential, m.e.p.c. decay was obviously biphasic, with two very distinct components (Maeno, 1966;Gage & Armstrong, 1968;Kordas, 1970;Deguchi & Narahashi, 1971;Maeno et al 1971;Katz & Miledi, 1975). Fig.…”

Section: Ph-dependence Of Procaine Actionmentioning

confidence: 99%

“…At the neuromuscularjunction, hyperpolarization increases the effects of externally applied procaine (Kordas, 1970; Deguchi & Narahashi, 1971;Maeno, Edwards & Hashimura, 1971; Adams, 1977), QX222 and QX314 (Beam, 1976;Neher & Steinbach, 1978; Ruff, 1982), curare and gallamine (Manalis, 1977;Katz & Miledi, 1978;Colquhoun, Dreyer & Sheridan, 1979;Colquhoun & Sheridan, 1981), tetraethylammonium (Adler, Oliveira, Eldefrawi, Eldefrawi & Albuquerque, 1979), decamethonium and hexamethonium (Adams & Sakmann, 1978;Milne & Byrne, 1981), atropine and scopolamine (Adler, Albuquerque & Lebeda, 1978), amantadine (Tsai, Mansour, Eldefrawi, Eldefrawi & Albuquerque, 1978) and histrionicotoxin (Albuquerque, Kuba & Daly, 1974). Since these drugs are all positively charged at physiological pH, the movement of drug into the channel seems to be enhanced as the inside of the fibre is made more negative.…”

Section: Introductionmentioning

confidence: 99%

Sites of action of procaine at the motor end‐plate.

Gage¹,

Hamill²,

Wachtel³

1983

The Journal of Physiology

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SUMMARY1. The effects of procaine at pH 7-4 and 9 9 were studied by examining the decay phase of spontaneous miniature end-plate currents (m.e.p.c.s) recorded from toad sartorius muscle fibres.2. Following exposure to procaine (005-01 mM) at pH 7 4, the decay of m.e.p.c.s rapidly became biphasic, and could be described as the sum of two exponential components.3. When the same concentrations of procaine were applied at pH 9 9, the development of biphasic m.e.p.c.s took much longer. Reversal of the effect upon washing out the procaine was much slower at pH 9.9 than at pH 7*4. 4. A rapid change in pH from 7-4 to 9-9 during exposure to a constant concentration of procaine quickly reduced the effect of procaine on m.e.p.c.s. The effect gradually returned after prolonged exposure to procaine at pH 9-9.5. These results suggest that procaine applied at high pH, where it is predominantly in uncharged form, may be diffusing to a site of action which is not directly accessible from the external surface of the membrane.6. The voltage-dependence of procaine action was similar whether it was applied at pH 7*4 or 9-9. 7. Intracellular injection of procaine rapidly produced biphasic m.e.p.c.s, whether the extracellular pH was 7-4 or 9-9. The effect of membrane potential on these m.e.p.c.s was similar to that seen for biphasic m.e.p.c.s produced by extracellular application of procaine.8. The results indicate that procaine can affect end-plate channels when applied to either surface of the muscle membrane, and that the voltage-dependence of procaine action does not arise from the influence of membrane field on the movement of charged procaine molecules into open channels.

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“…Local anaesthetics have also been shown to produce biphasic ACh potentials (Katz & Miledi, 1975). However, local anaesthetics must have a somewhat different action from barbiturates as unlike barbiturates, they produce biphasic endplate currents (Kordas, 1970). It must be emphasized that the decay time course of the endplate current is determined mainly by the conductance properites of the endplate channels, with the ACh concentration being near zero.…”

Section: Discussionmentioning

confidence: 99%