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Catecholamine neurotransmitters and the heart
Insights
Adrenaline may act as a cardiac neurotransmitter, with its effects on heart rate persisting long after infusion. This suggests adrenaline is taken up by nerve endings and influences heart rate via beta-presynaptic receptors.
Area of Science:
- Cardiology
- Neuropharmacology
Background:
- Adrenaline's role in cardiac function is complex.
- Investigating its potential as a neurotransmitter is crucial for understanding cardiovascular regulation.
Purpose of the Study:
- To explore adrenaline's function as a cardiac neurotransmitter.
- To determine the mechanisms underlying prolonged heart rate elevation after adrenaline infusion.
Main Methods:
- Infusion of adrenaline in 6 healthy volunteers.
- Assessing heart rate response to standing post-infusion.
- Evaluating effects of desipramine and alpha-methyl-p-tyrosine pretreatment.
Main Results:
- Heart rate remained elevated for hours post-infusion despite falling plasma adrenaline.
- Sympathetic stimulation (standing) caused a greater heart rate increase than control.
- Pretreatment with desipramine or alpha-methyl-p-tyrosine reduced or abolished these effects.
Conclusions:
- Adrenaline uptake into sympathetic nerve endings is key.
- Adrenaline influences heart rate via re-release and subsequent noradrenaline release.
- Evidence supports adrenaline's role in stimulating beta-presynaptic receptors.
Abstract:
The possible role of adrenaline as a cardiac neurotransmitter was studied following its infusion in 6 healthy volunteers. After the end of the infusion, heart rate remained elevated for several hours despite a rapid fall in plasma adrenaline concentration. Stimulation of sympathetic activity by standing caused a further marked increase in heart rate, which was greater than that found on a control occasion. These effects were abolished or reduced by pretreatment with either desipramine or (in the dog) alpha-methyl-p-tyrosine, suggesting that they depend both on uptake of the adrenaline into sympathetic nerve endings during infusion and on increased release of endogenous noradrenaline. These results are consistent with stimulation of the beta-presynaptic receptor by adrenaline when re-released from sympathetic nerves.