The goldfish (Carassius auratus) exhibits a remarkable capacity to survive and remain active under prolonged and severe hypoxia, making it a good model for studying cardiac function when oxygen availability is a limiting factor. Under hypoxia, the goldfish heart increases its performance, representing a putative component of hypoxia tolerance; however, the underlying mechanisms have not yet been elucidated. Here, we aimed to investigate the role of β3-adrenoreceptors (ARs) in the mechanisms

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... modulate goldfish heart performance along with the impact of oxygen levels. By western blotting analysis, we found that the goldfish heart expresses β3-ARs, and this expression increases under hypoxia. The effects of β3-AR stimulation were analysed by using an ex vivo working heart preparation. Under normoxia, the β3-AR-selective agonist BRL37344 (10-12 to 10-7 mol l-1) elicited a concentration-dependent increase of contractility that was abolished by a specific β3-AR antagonist (SR59230A; 10-8 mol l-1), but not by α/β1/β2-AR inhibitors (phentolamine, nadolol and ICI118,551; 10-7 mol l-1). Under acute hypoxia, BRL37344 did not affect goldfish heart performance. However, SR59230A, but not phentolamine, nadolol or ICI118,551, abolished the time-dependent enhancement of contractility that characterizes the hypoxic goldfish heart. Under both normoxia and hypoxia, adenylate cyclase and cAMP were found to be involved in the β3-AR-dependent downstream transduction pathway. In summary, we show the presence of functional β3-ARs in the goldfish heart, whose activation modulates basal performance and contributes to a hypoxia-dependent increase of contractility.