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Biomedical subjects

W Lippmann

Publications and source records attributed to W Lippmann.

At least 37 records · Page 2Linked to original sources
PubMed1977

Inhibition in the rat of gastric acid secretion and cyclic AMP analogs accumulation in vitro by somatostatin.

Various somatostatin (S) analogs exhibited similar degree and similar, or shorter, duration of inhibition of basal gastric acid secretion as S in the unanesthetized rat and similar, or less, inhibition of the cyclic AMP accumulation induced by prostaglandin E2 in the rat anterior pituitary in vitro. With the analogs examined, the gastrointestinal and pituitary receptors appear to exhibit generally similar recognition specificity with the differences within the gastro-intestinal activities reflecting duration of availability rather than receptor affinity.

Amino Acid Sequence↗
PubMed1977

Effect of butaclamol, a new neuroleptic, on serotoninergic mechanisms.

Butaclamol (1.0-0.1 mg kg-1, i.p.) and spiroperidol (1-0-0-5 mg kg-1, i.p.) but not (-)-butaclamol (15 mg kg-1, i.p.), blocked the hyperactivity induced in rats by tranylcypromine-L-tryptophan pretreatment. Neither butaclamol nor spiroperidol altered the accumulation of brain 5-HT following parglyine or the decline of brain 5-HT following inhibition with the tryptophan hydroxylase inhibitor alpha-propyldopacetamide thus indicating that butaclamol and spiroperidol do not affect either the synthesis or the turnover of brain 5-HT. It is concluded that the antagonism of the tranylcypromise-L-tryptophan-induced hyperactivity by butaclamol and spiroperidol is due to their blockade of dopaminergic receptors rather than an action on neuronal serotoninergic mechanisms.

Animals↗
PubMed1977

Synthetic melanocyte stimulating hormone release-inhibiting factor (MIF). Part III: effect of L-prolyl-N-methyl-D-leucyl-glycinamide and MIF on biogenic amine turnover.

The effect of the factor that inhibits the release of melanocyte stimulating hormone (MSH), i.e., L-prolyl-L-leucyl-glycinamide (MIF), and L-prolyl-N-methyl-D-leucyl-glycinamide, an analog, on brain norepinephrine (NE), dopamine (DA) and serotonin (5-HT) turnover was examined in rats. The analog (40 mg/kg i.p.), in a fashion similar to MIF (40 and 5 mg/kg i.p.), increased brain DA turnover; only MIF (40 mg/kg i.p.) increased endogenous DA levels. The analog (40 and 5 mg/kg i.p.) decreased brain NE turnover; MIF at the same doses was ineffective. Neither MIF nor the analog affected rat brain 5-HT turnover or the 5-HTP-induced behavioural syndrome in the mouse. These results indicate that the analog, like MIF, exerts effects on central catecholamine turnover. The different biochemical profile of the analog compared to MIF may be importance with regard to potential clinical use in the treatment of Parkinson's disease and depression.

5-Hydroxytryptophan↗
PubMed1976

Effects of pyrroxan and chlordiazepoxide on biogenic amine metabolism in the rat brain.

Pyrroxan (20 mg/kg, i.p.), a new potential antianxiety agent, increased brain norepinephrine (NE) turnover in rats, reflecting a possible central alpha-adrenergic receptor blocking activity. In contrast, chlordiazepoxide (20 mg/kg, i.p.), a widely used antianxiety agent, did not alter the NE turnover. Pyrroxan did not affect overall DA turnover although it did appear to accelerate DA turnover initially. The initial potentiation of DA turnover may indicate a short-lasting blocking action on DA receptors. In comparison, chlordiazepoxide (20 mg/kg, i.p.) decreased the turnover rate of DA. Effects of both drugs on 5-HT indicate a decrease in turnover with no significant monoamine oxidase activity or blockade of the 5-HT reuptake mechanism. Both drugs antagonized the decline in intraventicularly-injected 14C-5-HT. Neither drug caused consistent changes in endogenous 5-HT, 5-hydroxyindoleacetic acid, or tryptophan levels. Neither drug potentiated the behavioral effects of L-Dopa nor increased the 5-HTP behavoiral syndrome in the mouse. Pyrroxan may be expected to exhibit a spectrum of activity between that of minor and major tranquilizers, characterized by antianxiety action together with sedative or tranquilizing activity.

Animals↗
PubMed1976

Effects of tandamine and pirandamine, new potential antidepressants, on the brain uptake of norepinephrine and 5-hydroxytryptamine and related activities.

Two novel agents, tandamine (TA; a thiopyrano (3,4-b) indole) and pirandamine (PA; an indeno (2,1-c)pyran), and the tricyclic antidepressants desimipramine (DMI), imipramine (I) and amitriptyline (A) were compared in various in vivo pharmacological tests and for norepinephrine (NE) and 5-hydroxytryptamine (5-HT) neuronal uptake inhibition. TA was found to be equivalent, or greater, in activity to DMI in blocking brain NE uptake, antagonizing reserpine-induced effects and potentiating the behavioural effects of l-Dopa. Similarly to DMI, TA did not appreciably block brain 5-HT uptake; unlike DMI, TA did potentiate central 5-HT activity at high doses. PA exerted an opposite profile to TA, being equivalent to A and greater than I as a 5-HT uptake blocker and central 5-HT potentiator; PA was not effective as a NE uptake blocker or potentiator. Neither TA or PA exhibited in vivo MAO inhibition, and in contrast to DMI, I and A, exhibited no central anticholinergic effects. TA, but not PA, potentiated apomorphine-induced gnawing. These findings indicate that TA is a relatively specific blocker of neuronal NE uptake and PA is a selective 5-HT uptake blocker.

5-Hydroxytryptophan↗
PubMed1976

Dexclamol: effects on catecholamine metabolism and demonstration of stereochemical specificity of antagonism of central adrenergic receptors.

The effects of the benzocycloheptapyridoisoquinolinol derivative (+)-dexclamol-HCl and some of those of (+/-)-dexclamol and the corresponding (-)-dexclamol were compared to those of the potent neuroleptic agents droperidol and fluphenazine on norepinephrine (NE) and dopamine (DA) turnover in the whole brain and in the striatum of rats. Differences in NE and DA depletion following tyrosine hydroxylase inhibition with alpha-methyl-p-tyrosine indicated that (+)-dexclamol and droperidol increased DA turnover with no effect on NE turnover. At a higher dose both (+)-dexclamol and droperidol, but not (-)-dexclamol, accelerated DA turnover and also that of NE. A decrease in DA concentration occurred after both drugs under the latter condition only. (+)-Dexclamol, (+/-)-dexclamol and droperidol exhibited a similar onset of action employing striatal homovanillic acid (HVA) increase as indicative of DA turnover changes. The duration of action of droperidol was shorter than for (+)-dexclamol and (+/-)-dexclamol; fluphenazine displayed a slower onset and longer duration of activity. The (-)-dexclamol was ineffective. (+)-Dexclamol, droperidol and phentolamine reduced the concentrations of 3H-NE in heart when given after the 3H-NE, a probable indication of increased NE release due to adrenergic receptor blockade. The present findings demonstrate that the neuroleptic agent (+)-dexclamol, but not (-)-dexclamol, affects central DA and NE turnover and indicates a stereochemical specificity with respect to antagonism of central DA and NE receptors.

Animals↗
PubMed1975

Inhibition of prostaglandin E2-induced cyclic amp accumulation in the rat anterior pituitary by 11-deoxyprostaglandin E analogs (9-ketoprostynoic acids).

The effects of various 11-deoxyprostaglandin E analogs on the basal and prostaglandin E2 (PGE2)-induced cyclic AMP accumulation in the rat anterior pituitary were studied in vitro. 13-Hydroxy-9-oxoprost-14-ynoic acid at 5 X 10(-4)M but not 5 X 10(-5)M, decreased (45%) the induced accumulation and did not alter the basal accmulation; 15-hydroxy-9-oxoprost-13-ynoic acid at 5 X 10(-4)M caused less of a decrease (29%) in the induced and also did not alter the basal accumulation. (14Z)-13-Hydroxy-9-oxoprost-14-enoic acid at 5 X 10(-4)M did not alter the induced and caused a slight increase (5 fold) in the basal accumulation. 7-Oxa-13-prostynoic acid increased slightly the basal accumulation at 5 X 10(-5)M (2 fold) and 2.33 X 10(-4)M (6-fold) and did not antagonize the induced accumulation. Thus, the 9-ketoprostynoic acids are effective PGE2 antagonists in this system.

Animals↗