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• W27575035 startingPage "65" @default.
• W27575035 abstract "It is well established that adenosine and adenine nucleotides, such as ATP, are potent cardiac extracellular messengers whose actions are mediated by distinct cell surface receptors (A, and P2respectively). Adenosine, in addition to being a potent coronary vasodilator, also slows heart rate (negative chronotropic effect) and causes atrioventricular (AV) block (negative dromotropic effect) [1]. Adenosine also antagonizes the cardiac stimulatory actions (e.g. inotropic and arrhythmogenic) of ß-adrenergic agonists [1]. Adenine nucleotides such as ATP elicit several cardiovascular effects similar to those of adenosine [2]. The actions of ATP in the mammalian heart are to a large extent due to activation of A, and A2adenosine receptors by adenosine formed on degradation of this adenine nucleotide [2 3]. However, it has become increasingly clear that before its degradation to adenosine, extracellular ATP per se via activation of P2purinergic receptors (P2-receptors) causes a positive inotropic effect [4].KeywordsVentricular MyocytesAdenine NucleotideAction Potential DurationBayK 8644Atrial MyocytesThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves." @default.
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• W27575035 date "1995-01-01" @default.
• W27575035 modified "2023-09-26" @default.
• W27575035 title "Adenosine and Atp-Regulated Ion Currents in Cardiomyocytes" @default.
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• W27575035 doi "https://doi.org/10.1007/978-94-011-0117-2_7" @default.
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