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1

The action of antidepressant drugs administered during calcium channel blockade

100%
Vetulani J.
Polish Journal of Pharmacology
|
1993
|
vol. 45
|
issue 2
179-184
EN
This is an overview of the symposium concerned with the action of electroconvulsive treatment and some antidepressant drugs (mainly imipramine) applied during blockade of voltage-dependent calcium channels with nifedipine. The results in general suggest that a combination of calcium channel blockers with antidepressant drugs of ECT may be of clinical value in treatment of depression.
2

Phorbol ester and central chemosympathectomy augment beta-adrenoceptor response by different mechanisms

63%
Nalepa I., Vetulani J.
Polish Journal of Pharmacology
|
1993
|
vol. 45
|
issue 2
167-175
EN
The aim of this study was to compare the mechanisms of increased responsiveness of the beta-adrenoceptor dependent cyclic AMP generating system induced by chronic decrease of noradrenaline availability (beta-upregulation) with that resulting from simultaneous stimulation of alfa-adrnoceptors (alfa-potentiation) and to assess the role of portein kinase C in these phenomena. The beta-upregulation was produced by central chemosympathectomy with 6-hydroxydopamine>. The role of alfa1- and alfa2-adrenoceptors was assessed by comparison of the effects of specific beta-adrenoceptor agonist isoproterenol with those of a mixed alfa-beta-adrenoceptor agonist noradrenaline and clonidine was used to selectively stimulate alfa1-adrenoceptors. The role of protein kinase C was assessed by measuring cyclic AMP responses in the presence and absence of 12-O-tetradecanoyl-phorbol 13-acetate. The results indicate that the mechanism of increased responsiveness induced by central chemosympathectomy is different from the alfa-potentiation, that only alfa1-adrenoceptors are involved positively in alfa-potentiation, while the alfa1-adrenoceptors play an inhibitory role, and that increased responsiveness following central chemosympathectomy may be inhibited by protein kinase C activation.
3

The effect of calcium channel blockade on the action of chronic ECT and imipramine on responses of alpha-1 and beta-adrenoceptors in the rat cerebral cortex

63%
Nalepa I., Vetulani J.
Polish Journal of Pharmacology
|
1993
|
vol. 45
|
issue 2
201-205
EN
Chronic co-administration of nifedipine and ECT or imipramine results in an increase in responsiveness of cerebral cortical alfa1-adrenoceptor as measured by accumulation of inositol phosphate in cortical slices after noradrenaline stimulation; the responsiveness of beta-adrenoceptor, measured by accumulation of cyclic AMP, was depressed similarly by antidepressant treatment with and without nifedipine.
4

The effect of calcium channel blockade during electroconvulsive treatment on cerebral cortical adrenoceptor subpopulations in the rat

51%
Antkiewicz-Michaluk L., Michalik J., Romanska I., Vetulani J.
Polish Journal of Pharmacology
|
1993
|
vol. 45
|
issue 2
197-200
EN
Chronic administration of nifedipine (5 mg/kg/day for 10 days) induced some biochemical effects consistent with those of antidepressants: a significant depression in cortical alfa2-adrenoceptor density and reduction of beta-adrenoceptor affinity; nifedipine co-administration with electroconvulsive treatment potentiated the beta-downregulatory effect of the latter.
5

Electroconvulsive shock-induced impairment of spatial learning is aggravated by nifedipine

51%
Popik P., Mamczarz J., Vetulani J.
Polish Journal of Pharmacology
|
1993
|
vol. 45
|
issue 2
185-190
EN
Chronic electroconvulsive treatment applied immediately after a training session or with a 15 min delay impairs spatial learning and memory in the Morris water maze paradigm, and this impairment is not counteracted, but rather aggravated by co-administration of a calcium channel blocker, nifedipine.
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