Pharmacological studies of two new cardioselective adrenergic beta-receptor antagonists

Åblad, Bengt; Carlsson, Enar; Ek, Lars

doi:10.1016/0024-3205(73)90368-8

Cited by 194 publications

(58 citation statements)

References 8 publications

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“…In addition to pharmacological studies (Ablad, Carlsson & Ek, 1973;Carlsson, Dahlof, Hedberg, Persson & Tangstrad, 1977) radioligand binding studies revealed this coexistence. Hedberg, Minneman & Molinoff (1980) showed that Pl and P2-adrenoceptors were present in cat and guinea-pig right atria while the left ventricle of both species contained only P1-adrenoceptors.…”

Section: Introductionmentioning

confidence: 86%

β‐Adrenoceptors of the human myocardium: determination of β₁ and β₂ subtypes by radioligand binding

Heitz¹,

Schwartz

Velly

1983

British J Pharmacology

101

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Section: Introductionmentioning

confidence: 86%

β‐Adrenoceptors of the human myocardium: determination of β₁ and β₂ subtypes by radioligand binding

Heitz¹,

Schwartz

Velly

1983

British J Pharmacology

101

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“…However, a pretreatment with 15 mg/kg i.p. of the selective ␤-adrenergic antagonist metoprolol (Ablad et al 1973) failed to alter the degree of suppression induced by the same two doses of venlafaxine (two-way ANOVA, p ϭ .29) ( Figure 5). …”

Section: Effects Of Pre-treatments With (-)Pindolol and With Metoprolmentioning

confidence: 95%

Potentiation by (-)Pindolol of the Activation of Postsynaptic 5-HT1A Receptors Induced by Venlafaxine

Béı̈que

Blier

Montigny

et al. 2000

Neuropsychopharmacology

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The increase of extracellular 5-HT in brain terminal regions produced by the acute administration of 5-HT reuptake inhibitors (SSRI's) is hampered by the activation of somatodendritic 5-HT 1A autoreceptors in the raphe nuclei. The present in vivo electrophysiological studies were undertaken, in the rat, to assess the effects of the coadministration of venlafaxine, a dual 5-HT/NE reuptake inhibitor, and (-)pindolol on pre-and postsynaptic 5-HT 1A receptor function. The acute administration of venlafaxine and of the SSRI paroxetine (5 mg/kg, i.v.) induced a suppression of the firing activity of dorsal hippocampus CA 3 pyramidal neurons. This effect of venlafaxine was markedly potentiated by a pretreatment with (-)pindolol (15 mg/kg, i.p.) but not by the selective ␤ -adrenoceptor antagonist metoprolol (15 mg/kg, i.p .). That this effect of venlafaxine was mediated by an activation of postsynaptic 5-HT 1A receptors was suggested by its complete reversal by the 5-HT 1Aantagonist WAY 100635 (100 g/kg, i.v It is becoming increasingly clear that the therapeutic efficacy of antidepressant treatments such as selective serotonin reuptake inhibitors (SSRI's) finds its substrate in an enhanced serotonergic (5-HT) neurotransmission . At least in the rat, this occurs only in the midst of long-term administration of antidepressant treatments, which is necessary for the development of specific adaptative changes. Indeed, acute administration of SSRI's induces a reduction of firing activity of the 5-HT neurons of the raphe nuclei due to an increased activation of the somatodendritic 5-HT 1A autoreceptors, resulting from the increased extracellular 5-HT (de Montigny et al. 1981;Blier et al. 1984;Chaput et al. 1986;Hajós et al. 1995;Béïque et al. 1999). However, in the course of a long-term administration of SSRI's, 5-HT neurons recover their normal firing activity as a consequence of the desensitization of these autoreceptors . .). A short-term treatment with VLX (20 mg/kg/day ϫ 2 days) resulted in a ca. 90% suppression of the firing activity of 5-HT neurons in the dorsal raphe nucleus. This was prevented by the coadministration of (-)pindolol (15 mg/kg/day ϫ 2 days). Taken together, these results indicate that (-)pindolol potentiated the activation of postsynaptic 5-HTA way by which the action of the somatodendritic 5-HT 1A autoreceptors can be circumvented has been Activation of Postsynaptic 5-HT 1A Receptors 295 delineated by the electrophysiological observation that a 2-day administration of the mixed ␤ -adrenergic/5-HT 1A receptors antagonist (-)pindolol prevents the suppressant effects of paroxetine and of the 5-HT autoreceptor agonist LSD on the firing activity of dorsal raphe 5-HT (Romero et al. 1996). Although microdialysis studies cannot assess the postsynaptic impact, several such studies have corroborated the above by showing that the acute coadministration of (-)pindolol and an SSRI produces a greater elevation of extracellular levels of 5-HT in terminal regions than that achieved with the reuptake inhibitor alon...

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“…The clenbuterol-induced potentiation is apparently associated with P2-adrenoceptors, since it was completely inhibited by ICI 118,551, a p2-selective antagonist (Bilski et al, 1983), but was unaffected by metoprolol, an antagonist with pi-selective properties (Ablad et al, 1973). The ability of metoprolol to penetrate into the brain has been demonstrated by drug concentration measurements in brain tissue and in the CSF (Day et al, 1977;Cruickshank, 1980).…”

Section: Discussionmentioning

confidence: 99%

“…The aim of the study was to verify the involvement ofa central P-adrenoceptor by comparing the effects of the lipophilic p2-agonist clenbuterol (Kopitar & Zimmer, 1976) and the hydrophilic p2-agonist terbutaline (Bodin et al, 1972), and also to define the receptor subtype involved by subsequent blockade with the P,-selective antagonist metroprolol (Ablad et al, 1973) and the p2-selective antagonist ICI 118,551 (Bilski et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Central β‐adrenoceptors can modulate 5‐hydroxytryptamine‐induced tremor in rats

Hallberg¹

1986

British J Pharmacology

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1 The effects of two P2-adrenoceptor agonists with different lipophilicities were studied on tremor induced by L-5-hydroxytryptophan (L-5-HTP) in pargyline-and carbidopa-pretreated rats. 2 Tremor was recorded and analysed by an objective method based on accelerometry. 3 Clenbuterol, a lipophilic p2-selective agonist, dose-dependently enhanced tremor intensity, whereas the hydrophilic p2-agonist terbutaline had no effect.4 The clenbuterol-induced enhancement of tremor was completely abolished by the P2-selective antagonist ICI 118,551 but unchanged by the pi-selective antagonist metoprolol.5 The results suggest that centrally located P2-adrenoceptors can mediate a modulation of 5-hydroxytryptamine-induced tremor in rats.

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Pharmacological studies of two new cardioselective adrenergic beta-receptor antagonists

Cited by 194 publications

References 8 publications

β‐Adrenoceptors of the human myocardium: determination of β₁ and β₂ subtypes by radioligand binding

β‐Adrenoceptors of the human myocardium: determination of β₁ and β₂ subtypes by radioligand binding

Potentiation by (-)Pindolol of the Activation of Postsynaptic 5-HT1A Receptors Induced by Venlafaxine

Central β‐adrenoceptors can modulate 5‐hydroxytryptamine‐induced tremor in rats

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Pharmacological studies of two new cardioselective adrenergic beta-receptor antagonists

Cited by 194 publications

References 8 publications

β‐Adrenoceptors of the human myocardium: determination of β1 and β2 subtypes by radioligand binding

β‐Adrenoceptors of the human myocardium: determination of β1 and β2 subtypes by radioligand binding

Potentiation by (-)Pindolol of the Activation of Postsynaptic 5-HT1A Receptors Induced by Venlafaxine

Central β‐adrenoceptors can modulate 5‐hydroxytryptamine‐induced tremor in rats

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β‐Adrenoceptors of the human myocardium: determination of β₁ and β₂ subtypes by radioligand binding

β‐Adrenoceptors of the human myocardium: determination of β₁ and β₂ subtypes by radioligand binding