Effects of Sympathomimetic Amines on Neuromuscular Transmission

Bowman, W. C.; Raper, C.

doi:10.1111/j.1476-5381.1966.tb01665.x

Cited by 46 publications

(38 citation statements)

References 34 publications

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“…3). The anti-curare action of adrenaline has been attributed to presynaptic facilitatory action in acetylcholine quantal release (Bowman and Raper, 1966); this is similar to the mechanism that we considered in the anti-Mg++ action common to adrenaline and serotonin. The curare-potentiating action of adrenaline has been considered to reflect its postsynaptic hyperpolarising action (Bowman and Raper, 1966).…”

Section: Discussionsupporting

confidence: 76%

“…In this presynaptic action of serotonin, the alpha-adrenergic receptor was indicated to be the receptor as evidenced by the fact that its anti-Mg++ effect was prevented by an alpha-adrenergic blocker (phentolamine) but not by a beta-adrenergic blocker (propranolol) and a serotonergic blocker (lysergic acid diethylamide); this was similar to the presynaptic action of adrenaline ( Fig. 1) (Bowman and Raper, 1966). The anti-Mg++ action common to serotonin and adrenaline was also found with the administrations of dibutyryl cyclic AMP, caffeine, and calcium (Fig.…”

Section: Discussionmentioning

confidence: 60%

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Nerve, muscle, and serotonin.

Takamori¹

1977

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY Effects of serotonin on neuromuscular transmission and muscle contraction were studied in the tibialis anterior of rabbits. Serotonin antagonised the Mg++-induced block of transmission, and also provided dual effects on the curare-induced block, anti-curare phase followed by curare-potentiating phase. Independent of transmission processes, serotonin caused a reduction in twitch tension, mainly associated with decreased acceleration of twitch development. These serotonin actions were independent of vascular changes; pharmacological mechanisms are discussed in comparison with those of adrenaline and isoprenaline. A possible role of serotonin in causing a myopathy is proposed.A relationship between mammalian skeletal muscle and biogenic amine metabolism has been debated in relation to the pathogenesis of human muscular dystrophies. Abnormal contractile response to adrenaline (Takamori, 1975) and impaired activation of adenyl cyclase by adrenaline (Mawatari et al., 1974) suggest that adrenaline is implicated in abnormalities of the sarcoplasmic reticulum and plasma membrane in dystrophic muscles. Serotonin (5-hydroxytryptamine) is also one of the amines whose role is debated. It has been reported that an experimental myopathy similar to Duchenne muscular dystrophy was produced in the rat by ligation ofthe abdominal aorta and subsequent administration of serotonin (Mendell et al., 1971(Mendell et al., , 1972. It was presumed that the pargylineinduced myopathy, a model with histopathological features of Duchenne muscular dystrophy, was caused by an increased level of noradrenaline leading to excessive release of acetylcholine, or to an increased level of serotonin (Yu etal., 1974). Independent of vascular changes, Patten et al. (1974) demonstrated serotonin-induced depression of isometric twitch in rat skeletal muscles, and Meltzer (1976) suggested a direct effect of serotonin on rat skeletal muscles in causing myopathy. The present study attempts further to evaluate serotonin actions on neuromuscular transmission and muscle contraction. Investigations were performed in comparison with sympathomimetic amines and their antagonists, the pharmacological actions of which in the neuromuscular system are well known (Bowman and Nott,

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 60%

Nerve, muscle, and serotonin.

Takamori¹

1977

Journal of Neurology, Neurosurgery & Psychiatry

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“…8). This action appears to be different from that underlying the presynaptic action of adrenaline in neuromuscular transmission, for which the alpha-receptor is responsible (Bowman and Raper, 1966;Takamori et al, 1973). Two effects of adrenaline on muscle tissue, increased glycogenolysis and changes in contraction-relaxation cycle, have been postulated (Bowman and Nott, 1969;Marsden and Meadows, 1970;Rasmussen et al, 1972;Sullivan and Zaimis, 1973;Tashiro, 1973).…”

Section: Adrenaline Effects On Muscle Contractionmentioning

confidence: 99%

Contractility and supersensitivity to adrenaline in dystrophic muscle.

Takamori¹

1975

Journal of Neurology, Neurosurgery & Psychiatry

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“…Chronically denervated mammalian skeletal muscle has been shown to produce contractures to applied catecholamines both in vivo (Bowman & Raper, 1965;Turkanis, 1969) and in vitro (Bhoola & Schachter, 1961;Bhoola, Evans & Smith, 1972;Paterson, 1963). In normal muscles catecholamines do not cause contractures but affect indirectly evoked twitch tensions (Bowman & Raper, 1966). In the present investigation we have sought to elucidate the mechanism underlying this contractural 81 P PROCEEDINGS OF THE response and to demonstrate any association with the effects of catecholamines on normal muscle.…”

Section: Physiological Society April 1973mentioning

confidence: 99%

Proceedings of the Physiological Society, 13–14 April 1973, University of Southampton Meeting: Communications

1973

The Journal of Physiology

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3TUAll current techniques for the estimation of renin in plasma are indirect methods relying on measurement of angiotensin produced during incubation with renin substrate. These methods assess the enzymic activity of renin rather than the actual rate of renin secretion by the kidney because of the possible involvement of renin inhibitors or activators. We have recently developed a new renin assay based on the rocket immunoelectrophoresis technique of Laurell (1966). This measures renin concentration directly, and has been used in dogs to investigate the relationship between the amount of renin in plasma and its enzymic activity before and after partial occlusion of one renal artery. The contralateral artery was ligated.Ten mongrel dogs were used. After completion of the preparative procedures a 2 hr period was allowed for equilibration. At intervals during the succeeding two hours three plasma samples were collected from the renal vein for estimation of renin activity using ovine substrate (Skinner, 1967) and renin concentration using the new assay procedure. Renal blood flow was monitored with an electromagnetic flowmeter. In six of the dogs a constriction which reduced flow to 30-40 % of normal was then applied to the renal artery. Three further samples were collected during the ensuing 2 hr period. A similar protocol with no renal artery constriction was used in the four control dogs. A theoretical renin activity based on the renin concentration assays was calculated using the renin activity of the standard renin. The ratio, theoretical to actual activity, served as an assessment of the efficiency of angiotensin II production in the plasma.The pooled data from all the dogs show an increase in mean plasma renin activity from 8-05 renin units (s.x. 0.97) to 46-2 renin units (s.x. 9.0) 70 P PHYSIOLOGICAL SOCIETY, APRIL 1973 following renal artery constriction (P < 0.001). The corresponding renin concentration estimations were 0-27 units (S.E. 0 03) and 0-35 units (s.E. 0.03), and the difference was not significant. An alternative way of expressing these results is that the ratio of theoretical to actual renin activity fell from 91: 1 before to 22: 1 after renal artery occlusion. In the control animals over the same time course there were no significant changes in either renin activity or concentration.These data indicate that the well documented increase in plasma renin activity following partial renal artery occlusion is not due to increased renin secretion from the kidney but rather to change in its enzymic activity. A conceivable explanation could be based on changes in the availability of renin inhibitor (Smeby, Sen & Bumpus, 1967) but we have no direct evidence to support this against other possibilities. In the light of these observations the theories covering control of renin release should be regarded as relating to the control of plasma renin activity, and many of these situations need reinvestigation with this direct renin assay method. The mechanism by which angiotensin causes retention of sodium in...

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Effects of Sympathomimetic Amines on Neuromuscular Transmission

Cited by 46 publications

References 34 publications

Nerve, muscle, and serotonin.

Nerve, muscle, and serotonin.

Contractility and supersensitivity to adrenaline in dystrophic muscle.

Proceedings of the Physiological Society, 13–14 April 1973, University of Southampton Meeting: Communications

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