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At least 325 records · Page 18Linked to original sources
PubMed2001

British Pharmacological Society/The Physiological Society--joint meeting. Advances in glutamatergic pharmacology.

As befits the coming together of two major national societies, the Bristol meeting attracted a significant array of eminent pharmacologists and physiologists. This was reflected in the presentation of over 350 poster and oral communications stretching over the 3 days, with the host institution contributing substantially to the proceedings. A significant number of communications relating to glutamatergic transmission were presented, which will be the focus of this review. New information was disclosed relating to a novel class of metabotropic glutamate receptor modulators, recent advances in Glu(K5) compounds, AMPA/kainate and AMPA/NMDA receptor discriminators, and NMDA receptor subtype-selective compounds. Disclosures pertain to therapeutic areas including epilepsy, Parkinson's disease, cognitive enhancement, analgesia and psychosis.

Journal Article↗
PubMed1977

The pharmacology of a new hypoglycaemic agent N-[4-(2-(2,3-dihydrobenzo (b) furan-7-carboxamido)-ethyl)-benzenesulphonyl]-N'-cyclohexylurea (NOVO CS 476). II. Pharmacological studies on the mechanism of action.

The new sulphonylurea CS 476 does not potentiate the effect of insulin on plasma glucose levels in diabetic dogs in which an oral glucose load does not cause insulin release. In normal dogs propranolol 0.3 mg/kg intravenously inhibites the insulin release and the hypoglycaemia due to CS 476 suggesting involvement of beta-adrenergic receptors in its action on the pancreas. Pretreatment of dogs with phentolamine leads to an augmentation of the insulin response to CS 476.

Administration, Oral↗
PubMed1991

Pharmacology and clinical pharmacology of vigabatrin.

Vigabatrin is an enzyme-activated, irreversible inhibitor of gamma-aminobutyric acid (GABA) aminotransferase, which causes a marked increase in cerebral GABA concentration and a resulting anticonvulsant action. Recovery from its effects requires the synthesis of new enzyme, and this may take several days following a single dose. The pharmacokinetics of vigabatrin are not a good guide to its duration of action. It is cleared rapidly by renal elimination (giving a plasma half-life of approximately 7 to 9 hours), and therefore the effect of the drug long outlasts its presence in the body. Plasma drug level monitoring is therefore of little value in regulating vigabatrin therapy. The drug is not bound to plasma proteins. Interactions with other drugs would not be expected because of its predominant renal elimination and its lack of protein binding. Also, vigabatrin does not induce liver enzymes, as do many of the standard antiepileptic drugs. In several trials, however, a small but significant reduction in phenytoin levels has been seen following the addition of vigabatrin to the antiepileptic medication. The mechanism for this reduction in phenytoin levels has not yet been elucidated, though it does not appear to be of clinical significance.

4-Aminobutyrate Transaminase↗
PubMedDate not supplied

The pharmacology of new ethylenediamine derivatives (ROM-126, ROM-131, MK-142) with antiarrhythmic action. Part I. General pharmacological properties.

Mentioned compounds, studied on several species of animals, decrease blood pressure and the heart rate, modify catecholamine-induced effects, show properties characteristic for the beta-receptor blocking agents. The stated differences being due mainly to the power of their action. These compounds possess also spasmolytic and locally anaesthetic action of various degrees. Only ROM-131 has antihistamine action.

Adrenergic beta-Antagonists↗