Expression and functions of beta_1- and beta_2-adrenergic receptors on the bulbospinal neurons in the rostral ventrolateral medulla

摘要

The expression and effects of p-adrenergic receptors ((J-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 pi- and p2-ARs on the bulbospinal RVLM neurons electrophysiologically and histologically. To directly investigate whether RVLM neurons display sensitivity to metoprolol (a Pi-AR antagonist), dobutamine (a Pi-AR agonist), butoxamine (a P2-AR antagonist), and salbutamol (a P2-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 Pi- and p2-ARs on the RVLM neurons. To determine the presence of Pi-and p2-ARs histologically, immunofluorescence examination was performed. Five metoprolol-hyperpolarized neurons were examined for Pi-AR and tyrosine hydroxylase (TH) immunoreactivity. All of the neurons displayed Pi-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 Pi- and p2-AR immunoreactivity. Our findings suggest that Pi-AR antagonists or p2-AR agonists may decrease blood pressure through decreasing the activity of the bulbospinal RVLM neurons.