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- W2295384679 abstract "Chronic guanethidine treatment of rats (10 mg/kg/day for 13 weeks) resulted in depletion of catecholamine stores in the short adrenergic neurons supplying the vas deferens. This depleted state persisted for at least six months after cessation of treatment. Electron microscopy showed that the density of nerves supplying the smooth muscle of the vas deferens was normal, although the intra-axonal vesicles had lost their granular cores. These nerves had lost the ability to take up catecholamines, as shown by fluorescence histochemistry and their intra-axonal vesicles failed to take up 5-hydroxydopamine. The nerve-mediated response of the isolated vas deferens was greatly diminished and remained so for six months. However, its sensitivity to norepinephrine was increased 15-fold and even six months after cessation of treatment an 8-fold increase in sensitivity to norepinephrine remained. No increase in sensitivity to acetylcholine was observed. Cocaine rarely caused an increase in the responses of vasa deferentia from guanethidine-treated animals but greatly enhanced the responses of control vasa deferentia to a level comparable to that seen in vasa deferentia from treated rats. In contrast to the transient nonspecific postsynaptic supersensitivity produced by chronic reserpine treatment, the long-lasting supersensitivity to norepinephrine resulting from chronic guanethidine treatment appears to be largely presynaptic in origin, similar to that produced by surgical denervation or cocaine." @default.
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- W2295384679 date "1973-04-01" @default.
- W2295384679 modified "2023-09-23" @default.
- W2295384679 title "Long-lasting supersensitivity of the rat vas deferens to norepinephrine after chronic guanethidine administration." @default.
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