title: Tail arteries from chronically spinalized rats have potentiated responses to nerve stimulation in vitro.
abstract: Patients with severe spinal cord lesions that damage descending autonomic pathways generally have low resting arterial pressure but bladder or colon distension or unheeded injuries may elicit a life-threatening hypertensive episode. Such episodes (known as autonomic dysreflexia) are thought to result from the loss of descending baroreflex inhibition and/or plasticity within the spinal cord. However, it is not clear whether changes in the periphery contribute to the exaggerated reflex vasoconstriction. The effects of spinal transection at T7-8 on nerve- and agonist-evoked contractions of the rat tail artery were investigated in vitro. Isometric contractions of arterial segments were recorded and responses of arteries from spinalized animals ('spinalized arteries') and age-matched and sham-operated controls were compared. Two and eight weeks after transection, nerve stimulation at 0.1-10 Hz produced contractions of greater force and duration in spinalized arteries. At both stages, the alpha-adrenoceptor antagonists prazosin (10 nm) and idazoxan (0.1 microm) produced less blockade of nerve-evoked contraction in spinalized arteries. Two weeks after transection, spinalized arteries were supersensitive to the alpha(1)-adrenoceptor agonist phenylephrine, and the alpha(2)-adrenoceptor agonist, clonidine, but 8 weeks after transection, spinalized arteries were supersensitive only to clonidine. Contractions of spinalized arteries elicited by 60 mm K(+) were larger and decayed more slowly at both stages. These findings demonstrate that spinal transection markedly increases nerve-evoked contractions and this can, in part, be accounted for by increased reactivity of the vascular smooth muscle to vasoconstrictor agents. This hyper-reactivity may contribute to the genesis of autonomic dysreflexia in patients.
authors.affiliation: Prince of Wales Medical Research Institute, Randwick, NSW 2031, Australia. j.brock@unsw.edu.au
authors.forename: Melanie
authors.initials: M
authors.lastname: Yeoh
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 / Q000503:physiopathology*; D020211:Autonomic Dysreflexia / Q000503:physiopathology*; D002908:Chronic Disease; D003000:Clonidine / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D019329:Idazoxan / Q000494:pharmacology; D066298:In Vitro Techniques; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D013623:Tail / Q000098:blood supply; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D010656:Phenylephrine; D003000:Clonidine; D011188:Potassium; D011224:Prazosin; D019329:Idazoxan