title: Removal of half the sympathetic innervation does not reduce vasoconstrictor responses in rat tail artery.
abstract: Following reinnervation of denervated rat tail arteries, nerve-evoked contractions are at least as large as those evoked in normally innervated arteries despite a much lower nerve terminal density. Here nerve-evoked contractions have been investigated after transection of half the sympathetic innervation of normal tail arteries. After 1 week, the noradrenergic plexus 50-70 mm along the tail was about half as dense as control. Excitatory junction potentials recorded in smooth muscle cells of arterial segments isolated in vitro were half their normal amplitude. Surprisingly, nerve-evoked contractions of isometrically mounted segments were not reduced in amplitude, as was also the case after only 3 days. After 1 week, enhancement of nerve-evoked contractions by blocking either neuronal re-uptake of noradrenaline with desmethylimipramine or prejunctional α2-adrenoceptors with idazoxan was similar to control, suggesting that these mechanisms are matched to the number of innervating axons. The relative contribution of postjunctional α2-adrenoceptors to contractions evoked by long trains of stimuli was enhanced but that of α1-adrenoceptors was unchanged. Transiently, sensitivity to the α1-adrenoceptor agonist phenylephrine was slightly increased. After 7 weeks, amplitudes of nerve-evoked contractions remained similar to control, and sensitivity to phenylephrine had recovered but that to the α2-adrenoceptor agonist clonidine was slightly raised. The normal amplitude of nerve-evoked contractions after partial denervation is only partly explained by the greater contribution of α2-adrenoceptors. While the post-receptor mechanisms activated by nerve-released transmitter may be modified to amplify the contractions after partial denervation, our findings suggest that these mechanisms are normally saturated, at least in this artery.
authors.affiliation: Department of Anatomy and Neuroscience, University of Melbourne, Parkville, Vic. 3010, Australia.
authors.forename: Diana
authors.initials: D
authors.lastname: Tripovic
authors.forename: Elspeth M
authors.initials: EM
authors.lastname: McLachlan
authors.forename: James A
authors.initials: JA
authors.lastname: Brock
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000166:cytology / Q000294:innervation / Q000502:physiology*; D003000:Clonidine / Q000494:pharmacology; D003891:Desipramine / Q000494:pharmacology; D019329:Idazoxan / Q000494:pharmacology; D007537:Isometric Contraction; D009121:Muscle Denervation; D032389:Myocytes, Smooth Muscle / Q000502:physiology*; D009469:Neuromuscular Junction / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D009638:Norepinephrine / Q000378:metabolism; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D013564:Sympathetic Nervous System / Q000502:physiology*; D055366:Synaptic Potentials; D013623:Tail / Q000098:blood supply / Q000294:innervation; D014661:Vasoconstriction
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D010656:Phenylephrine; D003000:Clonidine; D003891:Desipramine; D009638:Norepinephrine; D019329:Idazoxan
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