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  • Title: Tail arteries from chronically spinalized rats have potentiated responses to nerve stimulation in vitro.
    Author: Yeoh M, McLachlan EM, Brock JA.
    Journal: J Physiol; 2004 Apr 15; 556(Pt 2):545-55. PubMed ID: 14766944.
    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.
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