The influence of temperature and anaemia on the adrenergic and cholinergic mechanisms controlling heart rate in the rainbow trout

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Abstract
The capacity for cardioacceleration by adrenergic and cholinergic mechanisms was studied in resting rainbow trout, Salmo gairdneri, at 5, 12, and 20 °C. The trout were fitted with chronic dorsal aortic catheters for heart rate and blood pressure measurements. At all three temperatures, muscarinic cholinergic blockade with atropine caused substantial tachycardia, thereby indicating the presence of cholinergic vagal tone in resting animals. The relative effect of atropine was significantly greater at 5 °C (+53% of resting heart rate) than at 12 and 20 °C (≈ +30%). Maximal adrenergic stimulation (via adrenaline) after atropine caused a small further cardioacceleration at all temperatures. The adrenaline effect increased significantly from +8% (of resting heart rate) at 5 °C to +15% at 20 °C. The findings provide qualified support for the hypothesis that a reduction in vagal cholinergic activity is relatively more important in tachycardia at low temperature, and that adrenergic stimulation is relatively more important at high temperature, although the cardioacceleratory capacity of the cholinergic mechanism remains dominant throughout. The increase in heart rate accompanying experimental anaemia (haematocrit ≤ 6%) at all three temperatures was almost entirely due to a removal of vagal cholinergic tone; the contribution of adrenergic mechanisms, if any, was small.