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The action of prednisolone at the neuromuscular junction was studied in mouse isolated phrenic nerve-diaphragm and rat external popliteal/sciatic nerve-tibialis anterior muscle preparations. Prednisolone (0.03 mM and 0.3 mM) did not alter the twitch-tension in phrenic nerve-diaphragm preparations after 120 min, but increased the frequency (170 +/- 4%) and amplitude (200 +/- 13%) of miniature end-plate potentials. Quantal content was not influenced by the glucocorticoid treatment. Prednisolone (400 microg/kg) did not change the twitch-tension in rat external popliteal/sciatic nerve-tibialis anterior muscle preparations. However, this steroid (0.3 mM) prevented the neuromuscular blockade by d-tubocurarine (1.45 microM) in mouse preparations by 70 +/- 10% (P0.05). A similar effect (82 +/- 6% protection, P0.05) occurred in rats treated with prednisolone (400 microg/kg) before d-tubocurarine (225 microg/kg). In phrenic nerve-diaphragm preparations, prednisolone (0.3 mM) increased (13 +/- 4%, p0.05) the twitch-tension in the presence of beta-bungarotoxin (1 microM), and prevented the blockade produced by this toxin (0.15 microM) in its third phase of action. This presynaptic facilitatory effect may contribute to the usefulness of prednisolone in myasthenia gravis.

The application of bradykinin to isolated segments of the epididymal or prostatic portion of the rat vas deferens increased the basal muscular tension mainly of the epididymal portion of the organ. Upon low frequency transmural electrical stimulation, the epididymal and the prostatic end of the organ both reacted to the application of bradykinin with an increase of twitch height. The increase in muscular tension observed in the epididymal portion of the ductus was resistant to tetrodotoxin but obliterated by 1 microM verapamil or nifedipine. The augmentation of the magnitude of the electrically driven muscle twitches was blocked by tetrodotoxin but not affected by 1 microM verapamil or nifedipine. Preincubation of the segments of the ductus with 10 microM indomethacin significantly reduced the increase in basal muscular tension caused by low concentrations of bradykinin but did not affect the electrically driven muscle twitches. Results suggest the existence of bradykinin receptors in the nerve endings of the adrenergic terminals of the organ and in the smooth muscle membrane. Whereas the neurogenic response found in both segments of the organ was of equal magnitude, the musculotropic response was predominantly found in the epididymal half of the organ.