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Biomedical subjects

A Uzan

Publications and source records attributed to A Uzan.

At least 91 records · Page 5Linked to original sources
PubMed1981

Central dopaminergic neurons during development of genetic and DOCA-salt hypertension in the rat.

The in vivo binding of [3H]spiroperidol was measured in discrete areas of the brain in 7-, 9- and 16-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto (WKY) controls. An increase in the [3H]spiroperidol binding in the striatum, tuberculum olfactorium and frontal cortex but not in the cerebellum was detected at all ages in SHR. The increase was more pronounced in 7- than in 9- or 16-week-old SHR. In vitro data indicated an increase in Bmax but no variation in Kd in the striatum of 7-week-old SHR. Moreover no difference was detectable in the dopaminergic cell bodies (A9, A10). This increase was specific to [3H]spiroperidol binding sites since no difference was observed in the in vivo binding of [3H]QNB and [3H]LSD in the same brain regions. No variation in dopamine level or dopamine utilization, as estimated by measuring the disappearance of the amine induced by alpha-methyl-p-tyrosine, was observed. The DOPA accumulation after injection of the DOPA decarboxylase inhibitor NSD 1015 was greater in the tuberculum olfactorium from 7-week-old SHR. An increase in [3H]spiroperidol binding sites was also observed in the striatum and tuberculum olfactorium after 7 weeks of DOCA-salt treatment. These results suggest that dopaminergic neurons might be implicated in the onset of hypertension in the rat.

Animals↗
PubMed1981

[Dopaminergic receptors on lymphocytes in idiopathic Parkinson's disease (author's transl)].

(3H) spiroperidol binding has been measured in lymphocytes from patients with Parkinson's disease and age matched healthy volunteers. A dramatic decrease (73 p. 100) in the number of binding sites Bmax without any variation of the affinity KD has been observed in untreated Parkinsonian patients. This decrease in Bmax is linearly correlated with the degree of disability of the Parkinsonian patients (r = 0.891, p less than 0.001). This decrease appeared to be relatively selective since no variation was observed with patients suffering of other neurological disorders. The possible relationships with the number of striatal dopamine receptors are discussed. With levodopa therapy, Bmax had the same mean value as in control subjects. This result means that levodopa induces an increase in lymphocyte binding sites and in five patients this increase could be observed by study before and during drug administration. In some severely disabled patients who had received levodopa for several years, Bmax was found much lower or higher than the mean value, which may suggest different interpretations of drug unefficiency.

Adult↗
PubMed1980

Tissue levels and displacement of in vivo labelled beta-adrenergic receptors by FM 24, an irreversible or slowly dissociable beta-blocker.

FM 24 [1-(2-exo-bicyclo[3,3,1]hept-2-ylphenoxy)-3-[(1-methylethyl)amino] 2-propanol hydrochloride] and propranolol were compared in mice with respect to their ability to displace in vivo 125I-hydroxybenzylpindolol which is selectively associated with beta-adrenergic receptor binding sites. After a simultaneous i.v. injection of the beta-blockers and 125I-hydroxybenzylpindolol propranolol was more active than FM 24. At an equiblocking dose i.e. a dose which inhibits by 80% the binding of 125I-hydroxybenzylpindolol, FM 24 was still effective after 6 h (40% inhibition in the brain and the heart, 60% in the lung) contrary to propranolol. After oral administration (2 mg/kg), 40% inhibition by FM 24 still persisted at 24 h in the heart whereas no effect of propranolol was detectable at 18 h. As the kinetics of [3H]FM 24 and [3H]propranolol after oral and i.v. administration are not very different we confirmed that the prolonged beta-blocking action of FM 24 was related to a tight irreversible binding to beta-receptors rather than to pharmacokinetic properties of this drug.

Adrenergic beta-Antagonists↗
PubMed1980

3-(4-Piperidinylalkyl)indoles, selective inhibitors of neuronal 5-hydroxytryptamine uptake.

A series of 3-(4-piperidinylalkyl)indoles was synthesized and tested as uptake inhibitors of biogenic amines. Some of these compounds are potent and very selective in blocking the 5-hydroxytryptamine (5-HT) uptake, as evidenced by biochemical data and behavioral tests. A discussion on structure-activity relationships is given. The most interesting member of the series, indalpine, 3-[2-(4-piperidinyl)ethyl]indole (1), was selected for clinical studies.

Animals↗
PubMed1979

Comparative distribution of two antidepressant drugs (imipramine and indalpine) in the rat as determined by analog computer simulation.

A ten-compartment analog computer model is presented to determine the precise distribution and excretion of two antidepressant drugs, LM 5008 AND Imipramine. Eight patterns were simulated using experimental data and drug distribution in the two undetermined compartments were obtained by the analog model. Close agreement with existing experimental data lends confidence in the model as a valuable tool for predictions in a variety of therapeutic situations.

Animals↗