title: Expression and functions of β1- and β2-adrenergic receptors on the bulbospinal neurons in the rostral ventrolateral medulla.
abstract: The expression and effects of β-adrenergic receptors (β-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 β1- and β2-ARs on the bulbospinal RVLM neurons electrophysiologically and histologically. To directly investigate whether RVLM neurons display sensitivity to 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 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 β1- and β2-ARs on the RVLM neurons. To determine the presence of β1- and β2-ARs histologically, immunofluorescence examination was performed. Five metoprolol-hyperpolarized neurons were examined for β1-AR and tyrosine hydroxylase (TH) immunoreactivity. All of the neurons displayed β1-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 β1- and β2-AR immunoreactivity. Our findings suggest that β1-AR antagonists or β2-AR agonists may decrease blood pressure through decreasing the activity of the bulbospinal RVLM neurons.
authors: Department of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama, Japan.
authors: Naoki
authors: N
authors: Oshima
authors: Department of Physiology, Showa University School of Medicine, Tokyo, Japan.
authors: Hiroshi
authors: H
authors: Onimaru
authors: Department of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama, Japan.
authors: Kojiro
authors: K
authors: Yamamoto
authors: Department of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama, Japan.
authors: Hanako
authors: H
authors: Takechi
authors: Department of Physiology, National Defense Medical College, Tokorozawa, Saitama, Japan.
authors: Yasuhiro
authors: Y
authors: Nishida
authors: Department of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama, Japan.
authors: Takashi
authors: T
authors: Oda
authors: Department of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama, Japan.
authors: Hiroo
authors: H
authors: Kumagai
mesh_terms: D058665:Adrenergic beta-1 Receptor Agonists / Q000494:pharmacology; D058671:Adrenergic beta-1 Receptor Antagonists / Q000494:pharmacology; D058666:Adrenergic beta-2 Receptor Agonists / Q000494:pharmacology; D058672:Adrenergic beta-2 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D066298:In Vitro Techniques; D008526:Medulla Oblongata / Q000166:cytology / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D018342:Receptors, Adrenergic, beta-1 / Q000096:biosynthesis* / Q000187:drug effects; D018343:Receptors, Adrenergic, beta-2 / Q000096:biosynthesis* / Q000187:drug effects; D013127:Spinal Nerves / Q000166:cytology / Q000378:metabolism*
chemical_list: D058665:Adrenergic beta-1 Receptor Agonists; D058671:Adrenergic beta-1 Receptor Antagonists; D058666:Adrenergic beta-2 Receptor Agonists; D058672:Adrenergic beta-2 Receptor Antagonists; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2