title: Effects of adrenoceptor antagonists on the cutaneous blood flow increase response to sympathetic nerve stimulation in rats with persistent inflammation.
abstract: There is some evidence that the sympathetic nervous system plays a role in the development and/or maintenance of painful states, and that sympathetic nervous function is altered in these conditions. Our previous experiments showed that electrical stimulation of the lumbar sympathetic trunk (sympathetic stimulation: SS), which normally induces a decrease in blood flow (BF) of plantar skin, induced its BF increase in about 50% of adjuvant-inflamed rats. To investigate the mechanism of this BF-increase response, we examined whether noradrenaline (NA) plays any role in this changed response to SS, and which receptor subtype is involved. We measured paw cutaneous BF response with a laser Doppler flowmeter in rats chronically inflamed with complete Freund's adjuvant. SS induced the BF-increase response in 50-67% of measured sites. Close-arterially injected NA induced the BF-increase response at dosages between 10-100 ng/kg only at the sites with the BF-increase response to SS. The BF-increase and -decrease responses to NA was significantly reduced after the close-arterial injection of either alpha1- or alpha2-adrenoceptor antagonists (p lt; 0.05, respectively). In contrast, although the BF-decrease responses to SS were significantly reduced by administration of alpha1- and alpha2-adrenoceptor antagonist, BF-increase response was reduced only by alpha1-adrenoceptor antagonist, and that only at a higher dose. In addition, the beta-adrenoceptor antagonist had no effects on both responses. These results suggest that the BF-increase response to SS involves, additionally to NA, a non-adrenergic mechanism.
authors.affiliation: Department of Neural Regulation, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chukusa-ku, Nagoya, 464-8601 Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Koeda
authors.forename: Jun
authors.initials: J
authors.lastname: Sato
authors.forename: Takao
authors.initials: T
authors.lastname: Kumazawa
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Tsujii
authors.forename: Kazue
authors.initials: K
authors.lastname: Mizumura
mesh_terms: D018674:Adrenergic Antagonists / Q000494:pharmacology*; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000528:radiation effects; D003872:Dermatitis / Q000503:physiopathology*; D004558:Electric Stimulation; D005528:Foot / Q000503:physiopathology; D006614:Hindlimb / Q000503:physiopathology; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology*; D051381:Rats; D011917:Rats, Inbred Lew; D012867:Skin / Q000098:blood supply / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D018674:Adrenergic Antagonists; D000316:Adrenergic alpha-Agonists; D011433:Propranolol; D009638:Norepinephrine; D011224:Prazosin