Beta 1 Adrenergic Receptors Decrease Glutamatergic Neurotransmission To Cardiac Vagal Neurons

β adrenergic receptors (βAR) are a frequent target for drugs used to treat cardiac arrhythmias, hypertension, as well as other heart conditions. One of the most commonly used drugs for treatment, β antagonists, act by blocking catecholamine binding sites in the heart, autonomic system as well as the kidneys. Despite the highly beneficial effect of β blockers in lowering heart rate and blood pressure, very little is known about the role of βAR in modulating parasympathetic activity that controls heart rate. In this study we examined, using patch clamp electrophysiology in-vitro, the effect of βAR on cardiac vagal neurons (CVNs), which are the neurons that dominate parasympathetic control of heart rate and originate in the brainstem nucleus ambiguus. Application of the β1 receptor subtype specific agonist dobutamine significantly decreased the frequency of excitatory postsynaptic currents (EPSCs) in CVNs. To determine the role of β2 receptors in altering glutamatergic EPSCs, albuterol, a β2 receptor agonist was applied. Albuterol did not evoke any significant change in excitatory glutamatergic neurotransmission to CVNs. These results suggest CVNs are inhibited by β1 but not β2 receptor activation, and that the beneficial effect of β receptor blockers in treating arrhythmias and tachycardia may include a disinhibition and increase in cardioprotective parasympathetic activity to the heart.