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- Ekstrom, J, et al.
(författare)
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Biochemical and functional evidence for nerve sprouting in the decentralized, hypertrophied rat urinary bladder
- 1987
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Ingår i: Pharmacology and Toxicology. - 1600-0773. ; 60:2, s. 86-89
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Tidskriftsartikel (refereegranskat)abstract
- The preganglionic nerves of the rat urinary bladder were cut. The decentralized bladders gained markedly in weight. Both one and four weeks post-operatively, transmural nerve stimulation evoked contractile responses of the muscle strips of the decentralized bladders, that were of the same magnitude as those of the control bladders. However, four weeks post-operatively, the atropine resistant fraction of the response was decreased; consequently, the atropine sensitive (cholinergic) fraction was increased. The activity of the acetylcholine synthesizing enzyme, choline acetyltransferase, was increased at the late time of observation. The present biochemical and functional findings may suggest outgrowth of branches from the decentralized post-ganglionic cholinergic nerves.
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- Ekström, J, et al.
(författare)
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Transient supersensitivity in the hypertrophied rat urinary bladder
- 1986
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 126:3, s. 365-370
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Tidskriftsartikel (refereegranskat)abstract
- The presence of a paraffin bolus intravesically for 1 or 4 weeks was accompanied by an approximate three-fold increase in bladder weight. A supersensitivity to methacholine was demonstrated in these hypertrophied bladders at 1 week but not at 4 weeks. At the earlier time of observation, the contractile responses in vitro to nerve stimulation were reduced, while at the later time of observation the responses were the same as those of controls; the atropine-sensitive fraction of the response was entirely responsible for the recovery. The concentration of choline acetyltransferase, indicating cholinergic nerve density and initially reduced by about 50%, rose in course of time. It is suggested that in the beginning of the experimental period, the muscle cells of the hypertrophied bladders in situ are exposed to 'subnormal' transmitter concentration. An extension of the field of innervation of the cholinergic nerves may explain the disappearance of the supersensitivity.
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