Regulation of adenosine formation by the heart.

Sparks, Harvey V.; Bardenheuer, Hubert J.

doi:10.1161/01.res.58.2.193

Cited by 190 publications

(70 citation statements)

References 70 publications

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“…& Physiological roles of cardiac P2X and P2Y purinoceptors [6][7][8][9][10][11][12][13][14][15][16]; & Roles of adenosine in health and disease [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35]; & Effects of ATP and adenosine on coronary myocytes [12,36]; & Purine degradation pathways in the myocardium [18,37] & Paroxysmal supraventricular tachycardia (PSVT) and fibrillation [60][61][62][63]. Broad reviews about purinergic signalling have been published that include a section about the heart [64-78].…”

Section: Introductionmentioning

confidence: 99%

Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

119

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This review is a historical account about purinergic signalling in the heart, for readers to see how ideas and understanding have changed as new experimental results were published. Initially, the focus is on the nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory nerves, as well as in intracardiac neurons. Control of the heart by centers in the brain and vagal cardiovascular reflexes involving purines are also discussed. The actions of adenine nucleotides and nucleosides on cardiomyocytes, atrioventricular and sinoatrial nodes, cardiac fibroblasts, and coronary blood vessels are described. Cardiac release and degradation of ATP are also described. Finally, the involvement of purinergic signalling and its therapeutic potential in cardiac pathophysiology is reviewed, including acute and chronic heart failure, ischemia, infarction, arrhythmias, cardiomyopathy, syncope, hypertrophy, coronary artery disease, angina, diabetic cardiomyopathy, as well as heart transplantation and coronary bypass grafts.

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Section: Introductionmentioning

confidence: 99%

Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

119

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“…6 Cardiac Actions ofAdenosine In the heart, in addition to causing coronary vasodilation, adenosine depresses sinoatrial (SA) node activity, AV nodal conduction, atrial contractility, and ventricular automaticity. Adenosine also attenuates the cardiac stimulatory actions of catecholamines and the release of norepinephrine from nerve terminals.1,3' Furthermore, adenosine inhibits oxygen metabolite generation by activated neutrophils and stimulates glycolysis.132 It is worth noting that the cardiac actions of adenosine are remarkably similar to those of the neurotransmitter acetylcholine (ACh).…”

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confidence: 99%

Cardiac electrophysiology of adenosine. Basic and clinical concepts.

1991

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Adenosine is an endogenous nucleoside that has potent electrophysiologic effects.1-4 As an antiarrhythmic agent, adenosine has several unique properties: 1) it is an intermediate metabolite (Figure 1), 2) it has a very short half-life (less than 1.5 seconds), 3) its effects are mediated by specific membrane receptors coupled to guanine nucleotide binding proteins (G proteins), and 4) it has sitespecific actions in the myocardium with important differential effects in supraventricular and ventricular tissue. ' Adenosine also has an important role in regulating the myocardial oxygen supply-demand balance. Adenosine achieves this by increasing oxygen supply through coronary vasodilation and by reducing oxygen demand by decreasing myocardial contractility, antagonizing the effects of catecholamines, and depressing automaticity and conduction within the sinus and atrioventricular (AV) nodes. ' Recently, the United States Food and Drug Administration approved the use of adenosine for therapy of paroxysmal supraventricular tachycardia (PSVT), the first clinical application of adenosine. The purpose of this review is to present a rational approach for the therapeutic applications of adenosine for cardiac arrhythmias based on an understanding of its cellular and integrative mechanisms of action.Adenosine System The essential components of the adenosine system in the heart are 1) a mechanism for formation of adenosine, 2) a receptor-effector complex, and 3) a mechanism for the removal of adenosine and the attenuation of its actions (Figure 2).1'5-7

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“…Furthermore, by attenuating the activity of previously stimulated adenylate cyclase, endogenous adenosine might also counter the positive inotropic and vasotonic effects of catecholamines, either administered exogenously or endogenously released by hypoxia, hypotension, and electrical shock. [25][26][27] Additional observations also suggest that endogenous adenosine may be released secondary to DC countershock alone. In normoxic, isolated, perfused guinea pig hearts, directly applied DC shock was found to significantly increase effluent levels of adenosine in an energy dose-dependent manner (Wesley and Belardinelli, unpublished observations).…”

Section: Discussionmentioning

confidence: 94%

Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression.

Wesley

Belardinelli

1989

Circulation

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In halothane-nitrous oxide-anesthetized pigs, the effect of the competitive adenosine antagonist, BW-A1433U (a derivative of 1,3-dipropyl-8-phenylxanthine), on postdefibrillation bradyarrhythmia and hemodynamic depression was investigated. In protocol 1, repetitive episodes of ventricular fibrillation lasting 15 seconds before transthoracic DC shock were performed in five animals, before (control) and after the administration of BW-A1433U (5 mg/kg i.v.). An unsuccessful initial shock was immediately followed by a rescue shock of 40 A. In ventricular fibrillation episodes requiring rescue shocks, nine of 19 episodes (47%) exhibited second-or third-degree atrioventricular block at 15 seconds postdefibrillation compared with only one of 16 BW-A1433U episodes (6%). In protocol 2, the efrect of BW-A1433U was determined in the presence of dipyridamole, a nucleoside uptake blocker known to potentiate the cardiac actions of adenosine. To counter the hypotensive effect of dipyridamole, methoxamine was continuously infused at 0.015 mg/kg/min i.v. Sequential episodes of ventricular fibrillation lasting 45 seconds were terminated by shocks of 40 A in the presence of methoxamine alone, after dipyridamole (1.5-7.5 mg i.v.), and after BW-A1433U (5 mg/kg i.v.). Over the first 15 seconds postdefibrillation, BW-A1433U significantly (p<0.05) increased the number of spontaneous beats (31±2) and systolic/diastolic blood pressure (111±4/67±5 mm Hg; mean+SEM; n=9) compared with both methoxamine (16±2 beats; 98±14/52+12 mm Hg; n=5) and dipynrdamole (8±3 beats; 58±11/27±6 mm Hg; n=9), respectively. Rapid infusion of BW-A1433U during dipyridamole postdefibrillation periods raised heart rate and blood pressure to preventricular fibrillation levels within 30 seconds. Thus, BW-A1433U can reverse and prevent postdefibrillation bradyarrhythmia and hemodynamic depression. Endogenous adenosine may be an important mediator of postdefibrillation cardiovascular collapse. (Circulation 1989;80:128-137) B radyarrhythmia and hypotension after ventricular defibrillation usually lead to a fatal outcome that is secondary to prolonged periods of inadequate tissue oxygenation and perfusion.1-3 Adenosine, an endogenous metabolite released during hypoxia and ischemia, exerts multiple depressant actions on cardiovascular function by activation of specific cell-surface receptors.4-10 Due to either cyclic AMP (cAMP)-independent (direct) or cAMP-dependent (indirect, antiadrenergic) actions, adenosine has been shown to relax vascular smooth muscle, reduce atrial and ventric-

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Regulation of adenosine formation by the heart.

Cited by 190 publications

References 70 publications

Cardiac purinergic signalling in health and disease

Cardiac purinergic signalling in health and disease

Cardiac electrophysiology of adenosine. Basic and clinical concepts.

Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression.

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