title: Complex cardiovascular actions of alpha-adrenergic receptors expressed in the nucleus tractus solitarii of rats.
abstract: Although both alpha(1)- and alpha(2)-adrenergic receptors (ARs) are known to be expressed in the nucleus of the solitary tract (NTS), the functional significance of these receptors is still not fully established. In this study, we microinjected alpha(1)- and alpha(2)-AR agonists into the NTS of urethane-anaesthetized Wister rats to study the cardiovascular effects in response to their activation. When the alpha(1)-AR agonist phenylephrine was microinjected into the area where barosensitive neurons are dominantly located (baro-NTS), mean arterial pressure (MAP) and heart rate (HR) were significantly elevated. When tested in the area where chemosensitive neurons are dominantly located (chemo-NTS), however, MAP and HR were significantly decreased. Pretreatment with the non-specific alpha-AR antagonist phentolamine into the NTS inhibited the phenylephrine-induced cardiovascular responses. In contrast, microinjection of the alpha(2)-AR agonist clonidine into either the baro-NTS or the chemo-NTS decreased MAP and HR; they were also inhibited by the alpha(2)-adrenergic antagonist yohimbine. Moreover, we immunohistochemically identified that cardiovascular responses induced by alpha(1)-ARs may be mediated by NTS neurons while those induced by alpha(2)-ARs may be mediated by astrocytes located in the barosensitive and chemosensitive areas of the NTS. These results suggest that both types of alpha-AR expressed in the NTS may be involved in regulating cardiovascular homeostasis via modulation of input signals from baroreceptor and chemoreceptor afferents; however, cardiovascular responses produced by stimulation of alpha(1)-ARs are strictly location specific within the NTS.
authors.affiliation: Department of Physiology, Wakayama Medical University School of Medicine, 811-1, Kimiidera, Wakayama City, 641-8509, Japan.
authors.forename: Mohammad E R
authors.initials: ME
authors.lastname: Bhuiyan
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Waki
authors.forename: Sabine S
authors.initials: SS
authors.lastname: Gouraud
authors.forename: Miwa
authors.initials: M
authors.lastname: Takagishi
authors.forename: He
authors.initials: H
authors.lastname: Cui
authors.forename: Toshiya
authors.initials: T
authors.lastname: Yamazaki
authors.forename: Akira
authors.initials: A
authors.lastname: Kohsaka
authors.forename: Masanobu
authors.initials: M
authors.lastname: Maeda
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology; D003000:Clonidine / Q000494:pharmacology; D020869:Gene Expression Profiling; D006339:Heart Rate / Q000187:drug effects; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D018340:Receptors, Adrenergic, alpha-1 / Q000235:genetics; D018341:Receptors, Adrenergic, alpha-2 / Q000235:genetics; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D011942:Receptors, Adrenergic, alpha; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D010656:Phenylephrine; D015016:Yohimbine; D003000:Clonidine; D010646:Phentolamine