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Chronic decentralization potentiates neurovascular transmission in the isolated rat tail artery, mimicking the effects of spinal transection
Author(s) -
Yeoh Melanie,
McLachlan Elspeth M.,
Brock James A.
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2004.074948
Subject(s) - idazoxan , prazosin , phenylephrine , medicine , methoxamine , stimulation , endocrinology , anesthesia , agonist , chemistry , anatomy , antagonist , receptor , blood pressure
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 α‐adrenoceptor antagonists prazosin (10 n m ) or idazoxan (0.1 μ m ) was reduced. Decentralized arteries were transiently supersensitive to the α 1 ‐adrenoceptor agonist phenylephrine and the α 2 ‐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 α,β methylene‐ATP, but the P2‐purinoceptor antagonist suramin (0.1 m m ) did not reduce nerve‐evoked contractions. Enlarged responses to 60 m m 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.