Chronic decentralization potentiates neurovascular transmission in the isolated rat tail artery, mimicking the effects of spinal transection.
Spinal cord transection produces a marked increase in the response of the isolated rat tail artery to sympathetic nerve stimulation, possibly as a result of a decrease in ongoing sympathetic activity. We have tested the effects of removing ongoing nerve activity on neurovascular transmission by cutting the preganglionic input to postganglionic neurones supplying the tail artery (decentralization). Isometric contractions to nerve stimulation were compared between decentralized arteries and those from age-matched and sham-operated controls. Nerve-evoked responses of decentralized arteries were much larger than those of control arteries at 2 and 7 weeks post operatively. The extent of blockade of nerve-evoked contraction by alpha-adrenoceptor antagonists prazosin (10 nM) or idazoxan (0.1 microM) was reduced. Decentralized arteries were transiently supersensitive to the alpha1-adrenoceptor agonist phenylephrine and the alpha2-adrenoceptor agonist clonidine; the unchanged sensitivity to methoxamine and phenylephrine after 2 weeks indicated no effect on the neuronal noradrenaline uptake transporter. Decentralized arteries were hypersensitive to alpha,beta methylene-ATP, but the P2-purinoceptor antagonist suramin (0.1 mM) did not reduce nerve-evoked contractions. Enlarged responses to 60 mM K+ after both 2 and 7 weeks were correlated with the response of the arteries to nerve stimulation, suggesting that increased postjunctional reactivity contributes to the enhanced contraction. Comparison between data from decentralized arteries and our previous data from spinalized animals showed that the two lesions similarly potentiate nerve-evoked contractions and have similar but not identical postjunctional effects. The enhanced vascular responses following a reduction in tonic nerve activity may contribute to the hypertensive episodes of autonomic dysreflexia in spinally injured patients.
Prince of Wales Medical Research Institute, Gate 1, Barker Street, Randwick, Sydney, NSW 2031, Australia.
Melanie
M
Yeoh
Elspeth M
EM
McLachlan
James A
JA
Brock
D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000502:physiology; D003000:Clonidine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D066298:In Vitro Techniques; D008159:Lumbar Vertebrae; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013116:Spinal Cord / Q000098:blood supply* / Q000187:drug effects / Q000502:physiology*; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D013623:Tail / Q000098:blood supply* / Q000187:drug effects / Q000502:physiology
D010656:Phenylephrine; D003000:Clonidine