title: The influence of beta-adrenergic activation on noradrenergic alpha1 activation of rabbit afferent arterioles.
abstract: The aim of the present investigation was to examine the effect of beta-adrenergic stimulation on smooth muscle calcium concentration ([Ca2+]i) in resting conditions and after administration of norepinephrine (NE) to stimulate alpha-adrenoceptors in isolated rabbit afferent arterioles loaded with the calcium-sensitive fluorescent probe fura-2. [Ca2+]i was evaluated in the proximal and distal parts of the arterioles. NE (4x10(-7) M) increased [Ca2+]i in both these regions. The alpha1-adrenoceptor antagonist prazosin (10(-7) M) totally abolished the NE-induced increase in [Ca2+]i, while the alpha2-adrenoceptor antagonist yohimbine (5x10(-7) M) had no influence on the response to NE. When beta-adrenoceptors were stimulated, using isoproterenol (10(-7) M), the NE-induced increase in [Ca2+]i was significantly lower in both regions. Activation of beta-adrenoceptors with isoproterenol did not affect the [Ca2+]i increase in response to depolarization with K+. Since beta-adrenoceptor stimulation raises the smooth muscle cell levels of cAMP, an adenylate cyclase stimulator, forskolin (10(-5) M) was administered prior to NE application. This maneuver also blunted the increase in [Ca2+]i in both regions. We conclude that the calcium response to NE in the isolated rabbit afferent arteriole is mediated by an alpha1-adrenoceptor. beta-Adrenoceptor stimulation and forskolin blunt the increase in [Ca2+]i induced by NE stimulation, indicating that cAMP counteracts the NE-induced activation of alpha1-adrenoceptors.
authors.affiliation: Department of Physiology, Uppsala University, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Kornfeld
authors.forename: M
authors.initials: M
authors.lastname: Salomonsson
authors.forename: A
authors.initials: A
authors.lastname: Gutierrez
authors.forename: A E
authors.initials: AE
authors.lastname: Persson
mesh_terms: D000262:Adenylyl Cyclases / Q000378:metabolism; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000344:Afferent Pathways; D000818:Animals; D001160:Arterioles / Q000294:innervation* / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D005456:Fluorescent Dyes; D016257:Fura-2; D007545:Isoproterenol / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000294:innervation* / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology*; D011224:Prazosin / Q000494:pharmacology; D011817:Rabbits; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects* / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D000317:Adrenergic alpha-Antagonists; D005456:Fluorescent Dyes; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D005576:Colforsin; D015016:Yohimbine; D000242:Cyclic AMP; D000262:Adenylyl Cyclases; D007545:Isoproterenol; D002118:Calcium; D016257:Fura-2; D009638:Norepinephrine; D011224:Prazosin