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• W2024507926 abstract "Catecholamines regulate cardiac function primarily by activating b1-adrenergic receptors (ARs) coupled to the stimulatory Gs protein and the cAMP/protein kinase A pathway. However, cardiomyocytes also express a1-ARs that exert important short-term effects on the rate, rhythm, and force of cardiomyocyte contraction. These acute a1-AR-dependent actions are a source of inotropic reserve during pathophysiological conditions such as heart failure, where b-ARs are downregulated and/or uncoupled from G proteins. a1-ARs also induce the morphologic and molecular changes that are considered hallmarks of cardiac hypertrophy. The intracellular signaling pathways activated by cardiomyocyte a1-ARs and their contribution to hypertrophic signaling have been scrutinized by several laboratories. In comparison, progress de®ning the biochemical and/or ionic mechanisms underlying a1-AR regulation of contraction has been relatively slow, at least in part due to the complexities of the regulatory controls activated by a1-ARs and the highly contextual nature of a1-AR signaling. For example, b1-ARs induce stereotypic rapid robust positive chronotropic, inotropic and lusitropic responses; in contrast, a1-AR-dependent modulation of contractile function varies substantially depending upon the species or age of the animal studied as well as the precise experimental conditions used for" @default.
• W2024507926 created "2016-06-24" @default.
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• W2024507926 date "2002-09-01" @default.
• W2024507926 modified "2023-09-24" @default.
• W2024507926 title "α1-Adrenergic Receptor Subtype Function in Cardiomyocytes: Lessons from Genetic Models in Mice" @default.
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• W2024507926 doi "https://doi.org/10.1006/jmcc.2002.2057" @default.
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