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Demonstrates that clonidine enhances potassium chloride-evoked purine efflux in rabbit pulmonary artery strips, suggesting an antiadenosine-mediated prevention of presynaptic autoinhibition.
1 The effect of clonidine on the 3H-purine release evoked by KCl or (-)-adrenaline was assessed in the superfused helical strip of the rabbit pulmonary artery pretreated with [3H]-adenosine. 2 Clonidine (3 x 10(-5) M to 10(-4) M) significantly enhanced the 3H-purine efflux evoked by 50 mM KCl but not by 3 x 10(-6) M) (-)-adrenaline. 3 This facilitatory effect of clonidine on the KCl-induced purine release was unaltered by phentolamine 3 x 10(-6) M. It was absent in arterial segments denervated with 6-hydroxydopamine 30 microgram/ml. 4 A sustained contractile response was evoked by clonidine 3 x 10(-5) M without an increase in the 3H-purine efflux. This was significantly reduced by phentolamine 3 x 10(-6) M, but not by yohimbine 10(-5) M or by denervation with 6-hydroxydopamine. 5 The uptake of [3H]-adenosine into the segments was not inhibited by clonidine 3 x 10(-5) M. 6 It is suggested that the facilitation by clonidine of the KCl-induced purine release is due to prevention of presynaptic autoinhibition of purine release from adrenergic nerves, by an antiadenosine action of the drug.
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Katsuragi et al. (1981) studied this question.
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