Abstract 444: Presence and Functions of B1- and B2-adrenergic Receptors on Bulbospinal Neurons in the Rostral Ventrolateral Medulla

Abstract

The presence and effects of β-adrenergic receptors (β-ARs) on bulbospinal RVLM neurons are little examined. To directly investigate whether RVLM neurons have sensitivity to propranolol (a non-selective β-AR antagonist), metoprolol (a β1-AR antagonist), dobutamine (a β1-AR agonist), butoxamine (a β2-AR antagonist), and salbutamol (a β2-AR agonist), we examined changes in the membrane potentials (MPs) of bulbospinal RVLM neurons using whole-cell patch-clamp technique, during superfusion with these drugs. During propranolol superfusion eight of 17 RVLM neurons were depolarized, and nine of 17 RVLM neurons were hyperpolarized. In contrast, during metoprolol superfusion sixteen of 20 RVLM neurons were hyperpolarized, and during dobutamine superfusion five of 6 RVLM neurons were depolarized. During butoxamine superfusion eleven of 16 RVLM neurons were depolarized, and during salbutamol uperfusion all of 8 RVLM neurons were hyperpolarized. To clarify the character of RVLM neurons by themselves, superfusion with metoprolol or butoxamine, dissolved in a low-Ca 2+ , high-Mg 2+ solution, was performed. During metoprolol superfusion nine of 12 RVLM neurons were again hyperpolarized, and during butoxamine superfusion seven of 8 RVLM neurons were depolarized. These results suggest that β1- and β2-ARs are actually present on the RVLM neurons. β1-AR antagonists decreased the activity of bulbospinal RVLM neurons, and β2-AR antagonists increased it. To determine the presence of β1- and β2-ARs histologically, immunofluorescent examination including double staining was performed. All of 5 metoprolol-hyperpolarized neurons showed β1-AR immunoreactivity, and all of 3 butoxamine-depolarized neurons showed β2-AR immunoreactivity. Furthermore, two RVLM neurons, which were depolarized during metoprolol superfusion and were hyperpolarized during followed butoxamine superfusion, were examined for β1- and β2-ARs immunoreactivity. These neurons showed immunoreactivity for both β1- and β2-ARs, and most β1-ARs immunoreactive neurons in the RVLM had immunoreactivity for β2-ARs.Our findings suggest that β1-AR antagonists or β2-AR agonists may decrease blood pressure through decreasing activity of bulbospinal RVLM neurons.