Toru Uozumi

Effect of metoclopramide-induced prolactin on aldosterone secretion in normal subjects.

Abstract We investigated the role of prolactin (PRL) on modurating the secretion of aldosterone in normal male subjects. Metoclopramide (5mg) which causes a significant rise of PRL was given by intravenous injection. The peak of PRL level at 30 min. after i.v. injection of metoclopramide (20.0 ± 1.6 ng/ml, mean ± S.E.) was significantly higher than the basal level (6.4 ± 2.1 ng/ml, P

INHIBITORY EFFECTS OF MYASTHENIC SERUM ON THE SYNTHESIS OF ACETYLCHOLINE IN THE RAT BRAIN

In 193416), Nevin reported the so called “myasthenic substance” which is contained in the serum of a patient with myasthenia gravis and disturbs the transmission of nerve impulses in the neuromuscular junction. This substance has since been investigated by Walkerze), Wilsonz’), Gross-Brockhoffll) and many other investigatorszo.zz.~3.24.2s). Although several systematic works have been made on the functional mechanism of this substance, no definite conclusion has been reached as to the problem whether this substance will interfere with the neuromuscular transmission by affecting the presynaptic site, by affecting the postsynaptic site and acting like curare which antagonizes acetylcholine(Ach), or by some other functional mechanism. While Struppler22.23), Wilson27) and Tsukiyama60) regarded the so-called “myasthenic substance” as a curare-like one which affects postsynaptic transmission, Windsorzs) suggested, in his preliminary report, that this substance has the effect of a depolarizing block on the neuromuscular junction and not a curare-like effect. Minot,ls), Desmedt4-7) et a12.3,9J3J4-17) suggested an inhibitory effect on the synthesis and the release of Ach in the presynaptic site on the basis of electrophysiological experiments but the evidence seems to be insufficient. We attempted to confirm whether the so-called “myasthenic substance” in serum has inhibitory effects on the synthesis of acetylcholine and affects the neuromuscular transmission at a presynaptic site. However, as it is impossible to examine the possible inhibitory effect of the myasthenic patient’s serum directly on the human neuromuscular junction, we conducted an experimental study using cerebral cortex slices obtained from rats in the attempt to elucidate whether the myasthenic patient’s serum may have an inhibitory action on the Ach synthesis induced after Quastel’s method’s).