Dopamine stimulation of cardiac <i>β</i>‐adrenoceptors: the involvement of sympathetic amine transporters and the effect of SKF38393

Habuchi, Yoshizumi; Tanaka, Hideo; Nishio, Manabu; Yamamoto, Taku; Komori, Toshiaki; Morikawa, Junichiro; Yoshimura, Manabu

doi:10.1038/sj.bjp.0701574

Cited by 22 publications

(14 citation statements)

References 35 publications

(49 reference statements)

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“…Dopamine has been reported to both inhibit and enhance the release of noradrenaline and to activate a-and b-adrenoceptors and dopamine receptors (Goldberg 1972;Habuchi et al, 1997). In the present study responses to dopamine were similar in Dbh À/À and Dbh þ /À mice.…”

Section: Change In Mean Arterialsupporting

confidence: 65%

Pressor responses to ephedrine are not impaired in dopamine β‐hydroxylase knockout mice

Liles

Baber

Deng

et al. 2007

British J Pharmacology

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Background and Purpose: Ephedrine and amphetamine can cause substantial increases in systemic arterial pressure. However, the role of endogenous noradrenaline release in mediating the pressor response to ephedrine is controversial. Studies using pharmacologic agents to decrease the synthesis, storage, and release of catecholamines have supported both a direct and an indirect mechanism of action for ephedrine. The purpose of the present study was to determine if endogenous noradrenaline release is required for cardiovascular responses to ephedrine and amphetamine using a genetic mouse model. Experimental Approach: Increases in systemic arterial pressure and heart rate in response to ephedrine and amphetamine were investigated and compared in dopamine b-hydroxylase knockout (Dbh -/-) mice that cannot synthesize noradrenaline. Dbh þ /-littermates have normal noradrenaline and adrenaline tissue levels, and served as controls in all experiments. Key Results: In Dbh -/-mice the increases in systemic arterial pressure and heart rate in response to i.v. injections of ephedrine were not impaired whereas responses to amphetamine were markedly reduced, when compared with responses in Dbh þ /-mice. The pressor response to tyramine was abolished whereas pressor responses to noradrenaline, phenylephrine, dopamine, and angiotensin II were similar in Dbh -/-and Dbh þ /-mice. Conclusions and Implications:The present results in Dbh -/-mice provide support for the hypothesis that pressor responses to ephedrine are directly mediated whereas responses to amphetamine are dependent on the release of noradrenaline and suggest that Dbh þ /-and Dbh -/-mice are useful for the study of direct and indirect mechanisms.

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Section: Change In Mean Arterialsupporting

confidence: 65%

Pressor responses to ephedrine are not impaired in dopamine β‐hydroxylase knockout mice

Liles

Baber

Deng

et al. 2007

British J Pharmacology

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“…At the concentrations used, only DA stimulated cAMP formation in NRCM by activation of b 1 -adrenoceptors. It is well documented that dopamine displays b-adrenoceptor agonism at higher concentrations (.3 mM), whereas cardiac effects at lower concentrations are attributed to DA-induced release of noradrenaline in vivo (Habuchi et al, 1997). The DA derivate NOD, in contrast, has no hemodynamic effects when applied in vivo (Lösel et al, 2010) but is more potent with regard to cytoprotection.…”

Section: Dopamine and Its Lipophilic Derivates Providementioning

confidence: 99%

Dopamine and Lipophilic Derivates Protect Cardiomyocytes against Cold Preservation Injury

Vettel

Hottenrott

et al. 2013

J Pharmacol Exp Ther

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Donor heart allografts are extremely susceptible to prolonged static cold storage. Because donor treatment with low-dose dopamine improves clinical outcome after heart transplantation, we tested the hypothesis that dopamine and its lipophilic derivate, N-octanoyl dopamine (NOD), protect cardiomyocytes from cold storage injury. Neonatal rat cardiomyocytes were treated with dopamine or NOD or left untreated and subsequently subjected to static cold storage (8-12 hours). Dopamine-and NOD-treated cardiomyocytes displayed a better viability compared with untreated cells after hypothermia. In untreated cardiomyocytes, cell damage was reflected by lactate dehydrogenase (LDH) release and a decrease in intracellular ATP. NOD was approximately 20-fold more potent than dopamine. Similarly to cardiomyocytes in vitro, rat hearts perfused with NOD before explantation showed significantly lower LDH release after static cold storage. ATP regeneration and spontaneous contractions after cold storage and rewarming only occurred in treated cardiomyocytes. Hypothermia severely attenuated isoprenaline-induced cAMP formation in control but not in dopamine-or NOD-treated cells. Esterified derivates of NOD with redox potential and lipophilic side chains reduced cell damage during cold storage similarly to NOD. In contrast to dopamine, neither NOD nor its derivates induced a significant b-adrenoceptor-mediated elevation of cellular cAMP levels. The b 1 -adrenoceptor antagonist atenolol and D 1 /D 2 receptor antagonist fluphenazine had no impact on the protective effect of NOD or dopamine. We conclude that dopamine as well as NOD treatment mitigates cold preservation injury to cardiomyocytes. The beneficial effects are independent of b-adrenoceptor or dopaminergic receptor stimulation but correlate with redox potential and lipophilic properties.

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“…6B, DA produced significant dose-related increases in HR in the normal preparation. This positive chronotropic effect of DA was reported to be produced via β-adrenoceptor [12,35]. After denervation with reserpine or 6-OHDA, the effect of DA was greatly suppressed (Fig.…”

Section: Dosementioning

confidence: 90%

Inotropic, Chronotropic, and Arrhythmogenic Effects of Dopamine on the Isolated Working Heart of Rabbit

Wakita¹

2007

J. Physiol. Sci

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Some improvements of Kodama's method for perfusing the isolated rabbit heart in its working mode were made. Increases in the right and left atrium pressure, together with an increase in the pulmonary artery pressure, were observed to occur immediately after the start of venous return, and then all of the increased pressures were found to remain at each constant level. In these stable states, the administration of dopamine (DA) into the perfusate was found to produce dose-related increases in contractile activities. In the preparations denervated with reserpine or 6-hydroxydopamine, in which tyramine (Ty) produced no response, the inotropic effectiveness of DA did not differ from that in the normal ones. On the other hand, responses to noradrenaline (NA) were found to increase significantly after the denervation. DA produced a dose-related increase in heart rates in the normal preparation, and this effect was greatly suppressed in the denervated preparations, suggesting that the primary chronotropic effect of DA is an indirect one via the release of NA from the sympathetic nerve terminals. Arrhythmogenic effects of NA, Ty or DA were also observed in these preparations. At all the doses tested, the incidence rates by NA were as high as 50% or more, the type of arrhythmia being recognized as atrial or ventricular extrasystole from the ECG analysis. On the other hand, the rates by DA were relatively low, less than 34%. From a comparison of the incidence rates between the normal and denervated preparations, this effect of DA was considered to be primarily an indirect one.Key words: isolated rabbit heart, perfusion method, inotropic effect of dopamine, chronotropic effect of dopamine, arrhythmogenic effect of dopamine.In regard to the methods for perfusing isolated mammalian heart preparations, Langendorff's is well known and has been used for more than 100 years for cardiovascular research in physiological, biochemical and/or pharmacological aspects [1,2]. In a heart perfused with this method, the retrograde perfusion via the cannulated aorta is designed to produce a constant flow or constant pressure in the aorta with no outflow or only mere outflow from the right or left ventricle, and there is no venous return except for a quite small amount of perfusate drainage via the coronary sinus to the right or left atrium. In this respect, Langendorff's preparation is not working.Kodama in 1961 attempted to convert the isolated rabbit heart preparation into a working mode by constructing an artificial venous and arterial circulation system using silicon and glass tubes and perfusing the heart via the vena cava and pulmonary vein to keep sufficient venous return to the ventricles [3][4][5][6]. In a heart thus perfused with a venous and arterial circulation system that is similar to that in vivo, the simultaneous recordings of perfusate pressures at the various parts of veins and arteries were possible, and it was recognized that the pressure of either the right or left ventricle exceeds that of the pulmonary or ao...

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Dopamine stimulation of cardiac β‐adrenoceptors: the involvement of sympathetic amine transporters and the effect of SKF38393

Cited by 22 publications

References 35 publications

Pressor responses to ephedrine are not impaired in dopamine β‐hydroxylase knockout mice

Pressor responses to ephedrine are not impaired in dopamine β‐hydroxylase knockout mice

Dopamine and Lipophilic Derivates Protect Cardiomyocytes against Cold Preservation Injury

Inotropic, Chronotropic, and Arrhythmogenic Effects of Dopamine on the Isolated Working Heart of Rabbit

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