Recherches sur la pseudo-cholinestérase du sérum et la cholinestérase vraie des globules rouges

Summary By means of a technic published in this journal (2, 66 [1946]), it has been observed that the activity of the pseudo-choline esterase of the serum is highest in presence of high concentrations of acetylcholine.The true choline esterase of the red corpuscules has her optimal activity at concentrations of 200 mg % acetylcholine. This high activity of these choline esterase is only going on during 3 to 5 minutes; after this period an inhibition occurs. At lower substrate concentrations (50 mg % acetylcholine) the difference in activity in the first and second phase is becoming less pronounced and the curve of the choline esterase activity becomes a straight line. At the small substrate concentration (4 mg % acetylcholine) again a primary higher choline esterase activity has been observed.Choline inhibitsin vitro the activity of the choline esterase. Prostigmine inhibits alsoin vivo andin vitro, the choline esterase of serum and globules.     

A negative inotropic effect of acetylcholine in the presence of several phosphodiesterase inhibitors

The phosphodiesterase inhibitors papaverine, theophylline and 3-isobutyl-1-methylxanthine (IBMX) reveal a negative inotropic effect of acetylcholine in cat ventricular heart muscle. This effect in unrelated to beta-adrenoceptor stimulation and possibly mediated by the accumulation of cyclic GMP.     

Der Einfluß von Desoxycorticosteron auf die Azetylcholinwirkung am isolierten Froschherz

Summary The action of desoxycorticosteronglucoside was tested on the isolated frog-heart. In concentrations of 10^–6 to 10^–4 a small negative inotropic effect is prevailing. Acting together with acetylcholine, the substance diminishes or abolishes the negative inotropic and chronotropic action of acetylcholine. Eserin has no influence and the inhibition is also observed with cholinchloride and the carbaminoyl ester of choline. This inhibitory action bears a close resemblance to the inhibitory action of thiamin. In both cases a complex mechanism seems to be involved.     

Stress by restraining potentiates morphine catalepsy in rats

Restraint-induced stress potentiated morphine catalepsy in rats. This potentiation was partially antagonized by pharmacologic treatments decreasing central serotonin, acetylcholine, prostaglandins and by naloxone. Selective increase in central dopamine also inhibited the potentiation.     

Effect of hydroxydopamine on the morphine-induced reduction in brain acetylcholine turnover

Morphine reduced brain acetylcholine turnover in normal and 6-hydroxydopamine-pretreated rats and mice. Morphine probably has a direct effect on cholinergic neurons rather than modifying acetylcholine indirectly through catecholamine neurons. Acetylcholine is not directly involved in morphine's antinociceptive action in the mouse but it could be implicated in the rat.     

Effect of hydroxydopamine on the morphine-induced reduction in brain acetylcholine turnover

Summary Morphine reduced brain acetylcholine turnover in normal and 6-hydroxydopamine-pretreated rats and mice. Morphine probably has a direct effect on cholinergic neurons rather than modifying acetylcholine indirectly through catecholamine neurons. Acetylcholine is not directly involved in morphine's antinociceptive action in the mouse but it could be implicated in the rat.     

Effects of chronic paralysis of chick embryo by flaxedil on the development of the neuromuscular junction]

Chronic paralysis of Chick embryos by the cholinergic antagonist flaxedil blocks the subsynaptic accumulation of acetylcholinesterase but not the formation of acetylcholine receptor cluster. Flaxedil paralysis also causes an increase of the total muscle content of acetylcholine receptor without altering the half-life of the receptor protein. The spontaneous activity of the embryon therefore "shuts off" the synthesis of extrasynpatic acetylcholine receptor.     

Effects of lithium chloride on peripheral acetylcholine release and brain acetylcholine levels in the guinea-pig.

Lithium chloride administered acutely or chronically to guinea-pigs had no effect on brain level of acetylcholine or on peripheral release of acetylcholine from longitudinal muscle of the ileum. The results suggest differences between in vitro and in vivo action of lithium.     

Effects of lithium chloride on peripheral acetylcholine release and brain acetylcholine levels in the guinea-pig

Summary Lithium chloride administered acutely or chronically to guinea-pigs had no effect on brain level of acetylcholine or on peripheral release of acetylcholine from longitudinal muscle of the ileum. The results suggest differences between in vitro and in vivo action of lithium.To whom correspondence should be addressed.     

The effect of physostigmine on (Na+ + K+)-ATPase activity in different rat brain regions

The activity of (Na+ + K+)-ATPase and acetylcholine esterase were followed in rat brain cerebral cortex, caudate, thalamus, hippocampus and medulla after i.v. administration of physostigmine. Both enzymes were found to be inhibited in a dose-dependent manner. The most pronounced inhibition of (Na+ + K+)-ATPase was found in caudate, where the highest activity of acetylcholine esterase is found.     

Activation of the electrogenic Na-pump of cardiac muscle fibres by ACh in K-free solutions

Summary The ionic mechanism of the membrane outward current (ACh-current) of bullfrog atrium muscle, induced by acetylcholine in K-free solution, was analyzed by a voltage-clamp experiment. The results suggested that the ACh-current was induced not only by an increase in K-conductance but also by an activation of the electrogenic Na-pump.Acknowledgment. This work was supported by a grant (257037) from the Ministry of Education of Japan.     

Pharmacology and function of the myoepithelial cell in the eccrine sweat gland.

Both acetylcholine and a Ca-ionophore, A23187, are comparatively strong stimulants of eccrine sweat secretion in vitro. Nevertheless, the contraction of the secretory coil was seen only after stimulation with acetylcholine but not with alpha or beta adrenergic drugs or with A23187. It was thus inferred that the myoepithelial contraction may not be playing an indispensable role in the overall process of eccrine sweat secretion.     

A negative inotropic effect of acetylcholine in the presence of several phosphodiesterase inhibitors

Summary The phosphodiesterase inhibitors papaverine, theophylline and 3-isobutyl-1-methylxanthine (IBMX) reveal a negative inotropic effect of acetylcholine in cat ventricular heart muscle. This effect is unrelated to -adrenoceptor stimulation and possibly mediated by the accumulation of cyclic GMP.I thank Mrs Petra Lauck for help. This work was supported by the Deutsche Forschungsgemeinschaft.     

Effects of thyroid state on brain stem responses to iontophoretic noradrenaline

Summary Responses to iontophoretic NA were increased in hyperthyroid rats and decreased in hypothyroid animals. No effect was observed on acetylcholine and glycine responses tested in the same way.This work was aided by grants from Consejo de Desarrollo Cientifico y Humanistico U.C.V. and CONICIT proyecto 51.26.SI-086.     

Microméthode potentiométrique pour la détermination de la cholinestérase

Summary A simple very sensitive and usefull method is described for the potentiometric micro-determination of the cholinesterase of blood serum, globules and tissues, using an ordinary potentiometer and an antimonium electrode. This method makes it possible to determine the cholinesterase in solutions of acetylcholine down to 3 mg %.     

Azelastine inhibits bronchial hyperreactivity to acetylcholine in guinea pigs

Contractile responses to acetylcholine were measured using isolated tracheae obtained from actively sensitized guinea pigs 0.5, 1, 5, 20, 24, 48 and 72 h after antigen challenge. Tracheal contractions to acetylcholine and to histamine were significantly increased 20 h but not 0.5, 1, 5, 24, 48 and 72 h after antigen challenge indicating bronchial hyperreactivity. When animals were pretreated with azelastine and then exposed to antigen challenge, concentration-response curve to acetylcholine did not differ from that obtained in control (non-challenged) tracheae. It is likely that azelastine is able to inhibit bronchial hyperresponsiveness to chemical mediators of bronchial asthma.     

Pharmacology and function of the myoepithelial cell in the eccrine sweat gland

Summary Both acetylcholine and a Ca-ionophore, A23187, are comparatively strong stimulants of eccrine sweat secretion in vitro. Nevertheless, the contraction of the secretory coil was seen only after stimulation with acetylcholine but not with alpha or beta adrenergic drugs or with A23187. It was thus inferred that the myoepithelial contraction may not be playing an indispensable role in the overall process of eccrine sweat secretion.Acknowledgment. The present study was supported by NIH grant 2R01AM 1625804.     

Über den Einfluss von Acetylcholin auf das Membranpotential denervierter Rattenzwerchfelle

Summary The membran potential of isolated rat-diaphragms has been measured by means of intracellular micro-electrodes, in order to study changes of the resting potential and of the depolarizing action of acetylcholine after section of the phrenic nerve. Within 80 days after denervation, the membrane potential was found to fall exponentially from 87 mV to 66 mV. The action of acetylcholine, on the other hand, was found to be independent of the duration of denervation: between the 4th and the 80th day of denervation: 10^–5g/ml acetylcholine always caused the membrane potential to fall by an average of the 9 mV.     

Der Einfluss von Acetylcholin auf die42Kalium-Abgabe postnataler,denervierter und reinnervierter Skeletmuskulatur

Summary The loss of⁴²K from the isolated rat diaphragm into the bathing solution is increased by acetylcholine, (a) 3 to 4 days after birth, (b) 7 to 14 days after sectioning of the phrenic nerve. The⁴²K loss is not altered by acetylcholine in the diaphragm of adult rats and after the denervated diaphragm has become reinnervated.     

Neuroactifs et tératogenèse vertébrale chez l'embryon d'oiseau

Summary Anticholinesterasic and depolarizing (analogues of acetylcholine) agents administered to quail embryos after 3 days of incubation give rise to vertebral fusions in addition to neck deformities. Antagonists of acetylcholine (gallamine and hexamethonium) produce only vertebral joint fusions. The incidence of all these compounds in the vertebral defects by the way of there neuroactive properties is proposed.