Cardiac β-adrenoceptor modulation by amiodarone

Nokin, Pierre; Clinet, M.; Schoenfeld, Philippe

doi:10.1016/0006-2952(83)90004-7

Cited by 60 publications

(28 citation statements)

References 17 publications

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“…However, saturation experiments performed in the absence and the presence of either amiodarone or SR 33589 demonstrated a decrease in Bmax without any effect on KD which is characteristic of a non-competitive inhibition. These effects were described previously for amiodarone (Nokin et al, 1983). SR 33589, which has similar interactions, is however more active than amiodarone.…”

Section: Discussionsupporting

confidence: 80%

“…These results were those generally expected in rat after amiodarone administration (Wiegand et al, 1986;Ceppi & Zaninovich, 1989;Perret et al, 1991). In contrast, SR 33589 treatment either had no effect on plasma thyroid hormones (50 and 100 mg kg-' day-) or induced a decrease in the T4/T3 ratio (150 mg kg-' day-) resulting from a decrease in T4 and probably due to treatment intolerance ( (Nokin et al, 1983;Plomp et al, 1985). Each drug was administered by oral route every 24 h for 14 days.…”

Section: Plasma Thyroid Hormone Levels and Cardiac Drug Concentrationmentioning

confidence: 99%

“…This was assessed by an in vitro rat cardiac membrane preparation following chronic treatment of the animals with SR 33589 and amiodarone. The rat was used as the effects of amiodarone chronic treatment on cardiac fiadrenoceptors and thyroid dysfunctions have been extensively studied in this animal species (Cohen-Armon et al, 1984;Colvin et al, 1989;Nokin et al, 1983;Perret et al, 1991;.…”

Section: Introductionmentioning

confidence: 99%

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Interaction of the antiarrhythmic agents SR 33589 and amiodarone with the β‐adrenoceptor and adenylate cyclase in rat heart

Chatelain¹,

Meysmans²,

Matteazzi³

et al. 1995

British J Pharmacology

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Section: Discussionsupporting

confidence: 80%

Section: Plasma Thyroid Hormone Levels and Cardiac Drug Concentrationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Interaction of the antiarrhythmic agents SR 33589 and amiodarone with the β‐adrenoceptor and adenylate cyclase in rat heart

Chatelain¹,

Meysmans²,

Matteazzi³

et al. 1995

British J Pharmacology

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“…None of the 30 patients, within 4 weeks of study, received a-adrenoceptor antagonists, P-antagonists or amiodarone which is claimed to have P-blocking properties (Nokin et al, 1983).…”

Section: Patient Characteristicsmentioning

confidence: 99%

The influence of atherosclerosis on the mechanical responses of human isolated coronary arteries to substance P, isoprenaline and noradrenaline

Berkenboom¹,

Depierreux

Fontaine³

1987

British J Pharmacology

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The responses to substance P. isoprenaline and noradrenaline were observed on human isolated coronary arteries removed from 30 human hearts, and were classified according to the age ofthe hearts, the presence or absence of cardiac failure and the degree of atherosclerosis.2 The endothelium-dependent vasodilator, substance P (0.1I M), relaxed rings precontracted with prostaglandin F2,, (PGF2,, 1 tM) when they were devoid of atherosclerosis. The presence of moderate or severe lesions of atherosclerosis abolished this response. There was no difference in the response, related to either the age of the hearts or to the presence or absence of cardiac failure. 3 The dose-response curves to isoprenaline (an endothelium-independent vasodilator) were also markedly altered by the presence of atherosclerotic lesions, while aging and the presence of cardiac failure did not alter the maximal relaxation. These last 2 factors induced only a rightward shift of the dose-response curves.4 On severely atherosclerotic rings, P-adrenoceptor-mediated responses were so altered that the effect of noradrenaline was wholly vasoconstrictor (via x-adrenoceptors). This response was not modified after pretreatment with atenolol (10 PM).5 It is concluded that atherosclerosis in human coronary arteries, induces alterations in the responses to substance P and to P-adrenoceptor agonists. The P-adrenoceptor-mediated relaxations seem more influenced by the presence of atherosclerosis than they are by aging or by the down-regulation induced by cardiac failure. Conversely, the x-adrenoceptor responses appear to be well preserved.

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“…ofthe action ofthe drug on the heart, resembling those of hypothyroidism, have been described since 1970; the reduced heart rate (Charlier, 1970;Ferrero et al, 1981) appears to result from a direct electrophysiological effect on the pacemaker cells ofthe sinus node although the non-specific adrenergic blocking activity of the drug may also be involved (Polster & Broekhuysen, 1976). A decrease in the density of Padrenoceptors at the myocardial cell surface (Nokin et al, 1983;Sharma & Corr, 1983) and a reduction in myocardial oxygen consumption (Harris et al, 1986) have been demonstrated: the latter has been shown to be dose-related in the dog. Other effects include an increase in the ratio of V3 to VI myosin heavy chain isoenzymes (this could be reversed by the administration of T3) (Wiegand et al, 1984), a reduction in cardiac myosin-ATPase (Sogol et al, 1983) and a reduction in Na', K+-ATPase activity in rabbit and guinea-pig heart .…”

Section: Discussionmentioning

confidence: 99%

Effects of amiodarone and thyroid dysfunction on myocardial calcium, serum calcium and thyroid hormones in the rat

Gammage

Franklyn

Logan³

1987

British J Pharmacology

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1 Myocardial calcium content was found to be elevated and serum calcium reduced in hypothyroid rats.2 Treatment of rats with amiodarone at either 30mg kg-' or 150mg kg-' daily did not result in any significant changes in myocardial or serum calcium. 3 The administration of amiodarone to hypothyroid rats attenuated the changes in serum but not myocardial calcium, suggesting that amiodarone may exert a thyroid hormone-like effect in the hypothyroid state. 4 The administration of amiodarone to thyroid hormone-treated rats resulted in attenuation of the effects on serum calcium and calculated intracellular calcium; this was consistent with an antagonistic interaction between amiodarone and thyroid hormones. 5 Administration of amiodarone resulted in significant changes in circulating thyroid hormone levels in the rat; triiodothyronine was reduced and basal thyrotrophin elevated compared to euthyroid controls. Serum thyroxine was not changed; this is in contrast to the effects in man. 6 Amiodarone does not exert its anti-arrhythmic action via changes in total myocardial calcium content in the euthyroid rat; nonetheless the described interactions between the drug and thyroid hormones may be involved in its mechanism of action.

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Cardiac β-adrenoceptor modulation by amiodarone

Cited by 60 publications

References 17 publications

Interaction of the antiarrhythmic agents SR 33589 and amiodarone with the β‐adrenoceptor and adenylate cyclase in rat heart

Interaction of the antiarrhythmic agents SR 33589 and amiodarone with the β‐adrenoceptor and adenylate cyclase in rat heart

The influence of atherosclerosis on the mechanical responses of human isolated coronary arteries to substance P, isoprenaline and noradrenaline

Effects of amiodarone and thyroid dysfunction on myocardial calcium, serum calcium and thyroid hormones in the rat

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