Expression and functions of β1- and β2-adrenergic receptors on the bulbospinal neurons in the rostral ventrolateral medulla

The expression and effects of beta-adrenergic receptors (beta-ARs) on the neurons of the bulbospinal rostral ventrolateral medulla (RVLM) have been limitedly examined to date. The objective of this study was to examine the expression of beta(1)-and beta(2)-ARs on the bulbospinal RVLM neurons electrophysiologically and histologically. To directly investigate whether RVLM neurons display sensitivity to metoprolol (a beta(1)-AR antagonist), dobutamine (a beta(1)-AR agonist), butoxamine (a beta(2)-AR antagonist), and salbutamol (a beta(2)-AR agonist), we examined changes in the membrane potentials of the bulbospinal RVLM neurons using the whole-cell patch-clamp technique during superfusion of these drugs. During metoprolol superfusion, 16 of the 20 RVLM neurons were hyperpolarized, and 5 of the 6 RVLM neurons were depolarized during dobutamine superfusion. During butoxamine superfusion, 11 of the 16 RVLM neurons were depolarized, and all of the 8 RVLM neurons were hyperpolarized during salbutamol superfusion. These results suggest the expression of beta(1)-and beta(2)-ARs on the RVLM neurons. To determine the presence of beta(1)- and beta(2)-ARs histologically, immunofluorescence examination was performed. Five metoprolol-hyperpolarized neurons were examined for beta(1)-AR and tyrosine hydroxylase (TH) immunoreactivity. All of the neurons displayed beta(1)-AR immunoreactivity, whereas three of the neurons displayed TH immunoreactivity. All of the five RVLM neurons that became depolarized during metoprolol superfusion and hyperpolarized during butoxamine superfusion displayed beta(1)-and beta(2)-AR immunoreactivity. Our findings suggest that beta(1)-AR antagonists or beta(2)-AR agonists may decrease blood pressure through decreasing the activity of the bulbospinal RVLM neurons.