Effects of endothelium-derived catecholamines on heart rate, blood pressure and gill ventilation in the rainbow trout

In most fish and tetrapods, regulation of cardiovascular system is traditionally attributed to the actions of the sympathetic and parasympathetic nervous systems on the heart and vasculature. Beyond the classic neurotransmitters (adrenaline, noradrenaline, and dopamine), the vascular endothelium can synthesize newly discovered catecholamines that modulate vascular tone and cardiac function independently of neuronal release, but their cardiorespiratory effects in fish remain unknown. Therefore, we characterized the cardiorespiratory responses of conscious rainbow trout (Oncorhynchus mykiss; n = 18) to ultra-low doses (100 fmol/kg to 10 nmol/kg) of 6-nitrodopamine (6-ND), 6-cyanodopamine (6-CYD), and 6-nitroadrenaline (6-NADR), comparing them to classical catecholamines (dopamine and adrenaline; 10 nmol/kg). The order of injection was randomized. Then, α₁-adrenoceptor blockade with prazosin (2.38 μmol/kg) was performed and a single 10 nmol/kg bolus challenge of the newly discovered catecholamine, adrenaline and dopamine in a random order. Fish were instrumented with a dorsal aortic catheter to allow bolus drug administration and measurement of mean arterial pressure and heart rate, as well as a buccal cannula to monitor ventilatory rate and amplitude. All three newly discovered catecholamines induced hypertension and concomitant bradycardia, with significant effects even at the lowest doses. Prazosin abolished bradycardia to 6-NADR, as well as the effects of adrenaline. In contrast, the hypertensive and bradycardic responses to 6-ND, 6-CYD, and dopamine were unaffected. None of the catecholamines affected ventilation. We provide new in vivo evidence that ultra-low doses of 6-substituted catecholamines elevate arterial pressure and trigger bradycardia via α₁-adrenoceptor independent mechanisms, suggesting alternative vascular pathways and a potential physiological role in fish.