title: Sympathetic vasoconstriction is potentiated in arteries caudal but not rostral to a spinal cord transection in rats.
abstract: Sympathetic nerve-mediated contractions of mesenteric and tail arteries controlled by preganglionic neurones decentralized by a spinal cord injury (SCI) are potentiated, and likely contribute to autonomic dysreflexia. However, reactivity to the α(1)-adrenoceptor agonist phenylephrine has been reported to be enhanced in vascular beds controlled by preganglionic neurones lying both rostral and caudal to an SCI in vivo. Here responses of isometrically-mounted median and saphenous arteries isolated from rats 2 and 8 weeks after transection of the T4 spinal cord have been compared with those from sham-operated rats. After SCI, contractions of median arteries to perivascular nerve stimulation, to α-adrenoceptor agonists (phenylephrine and clonidine), to the P2X-purinoceptor agonist α,β-methylene ATP, and to 60 mM K(+) were unchanged. Blockade of nerve-evoked contractions by α-adrenoceptor antagonists (prazosin and idazoxan) was not affected by SCI in either the median or saphenous arteries. In contrast, at 2 and 8 weeks after SCI, nerve-evoked contractions of saphenous arteries were potentiated. Saphenous arteries were less sensitive to phenylephrine 8 weeks after SCI, and their contractions to 60 mM K(+) were reduced. However, the sensitivity of saphenous arteries to clonidine was unchanged by SCI. Eight weeks after SCI, the reactivity of saphenous arteries to α,β-methylene ATP was unchanged, but the P2-antagonist suramin produced more blockade of nerve-evoked contractions. These findings demonstrate that neurovascular transmission is enhanced in arteries located caudal, but not rostral, to a spinal transection. In the saphenous artery, the most likely explanation seems to be an increase in neurotransmitter release, as may occur in other inactive sympathetic pathways caudal to the lesion.
authors.affiliation: Spinal Injuries Research Centre, Prince of Wales Medical Research Institute, University of New South Wales, Sydney, New South Wales, Australia.
authors.forename: Nicole M
authors.initials: NM
authors.lastname: Rummery
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 / Q000294:innervation / Q000502:physiology*; D003000:Clonidine / Q000494:pharmacology; D003627:Data Interpretation, Statistical; D004558:Electric Stimulation; D005260:Female; D009119:Muscle Contraction / Q000502:physiology; D009213:Myography; D010656:Phenylephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D058919:Purinergic P2 Receptor Antagonists / Q000494:pharmacology; D058911:Purinergic P2X Receptor Agonists / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013116:Spinal Cord / Q000098:blood supply*; D013119:Spinal Cord Injuries / Q000473:pathology*; D013268:Stimulation, Chemical; D013498:Suramin / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014661:Vasoconstriction / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D058919:Purinergic P2 Receptor Antagonists; D058911:Purinergic P2X Receptor Agonists; D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D013498:Suramin; D011189:Potassium Chloride; D003000:Clonidine; D011224:Prazosin