Hypertrophy of the rat urinary bladder following reduction of its functional volume

Peterson, Christine; Goss, Richard J.; Atryzek, Vladimir

doi:10.1002/jez.1401870113

Cited by 19 publications

(7 citation statements)

References 11 publications

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“…1983). Other investigators have induced hypertrophy by placing a bolus of paraffin chronically into the bladder (Peterson et al 1974), or simply by repeatedly injecting fluid into the organ (Carey 1921). Compression or ligature is used to induce hypertrophy of the ureter (Lange 1940).…”

Section: Experimental Models In Laboratory Animalsmentioning

confidence: 99%

Hypertrophy of visceral smooth muscle

Gabella

1990

Anat Embryol

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Smooth muscles of viscera undergo a large increase in volume when there is a chronic, partial obstruction impairing the flow of lumenal contents. Hypertrophy of smooth muscle occurs in various medical conditions and several methods are available for inducing it experimentally in laboratory animals, especially in urinary bladder, small intestine and ureter. The hypertrophic response differs somewhat with the type of organ, the animal species, the age of the subject, and the experimental procedure. Ten- to fifteen-fold increases in muscle volume develop within a few weeks in the urinary bladder or the ileum of adult animals, a growth that would not have occurred in the lifespan of the animal without the experimental intervention. The general architecture of the muscle and the boundaries with adjacent tissues are well preserved. In intestinal hypertrophy, muscle cells increase in number: mitoses are found in mature, fully differentiated muscle cells. Cell division by full longitudinal splitting of muscle cells may also occur. Enlargement of muscle cells accounts for most of the muscle hypertrophy. The hypertrophic muscle cell has an irregular profile with deep indentations of the cell membrane, bearing caveolae and dense bands; however, the cell surface grows less than the cell volume (reduction of surface-to-volume ratio). The nucleus is crenated and is much less enlarged than the cell (reduction of the nucleo-plasmatic ratio). Mitochondria grow in number but in some muscles their spatial density decreases; intermediate filaments increase more than myofilaments. The spatial density of sarcoplasmic reticulum is generally increased. In the hypertrophic intestine, gap junctions increase in number and size; in the bladder, gap junctions are absent both in control and in hypertrophy. Thus the hypertrophic muscle cell is not only larger than a control cell, but has a different pattern of its structural components. Extensive neo-angiogenesis maintains a good blood supply to the hypertrophic muscle. The density of innervation is much decreased in the hypertrophic intestine, whereas it appears well maintained in the bladder. Neuronal enlargement is found in the intramural ganglia of the intestine and in the pelvic ganglion. The mechanisms involved in hypertrophic growth are unknown. Three possible factors, mechanical factors, especially stretch, altered nerve discharge, and trophic factors are discussed.

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Section: Experimental Models In Laboratory Animalsmentioning

confidence: 99%

Hypertrophy of visceral smooth muscle

Gabella

1990

Anat Embryol

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“…Gabella 1975, Johansson 1975. The urinary bladder hypertrophies following injection of paraffine into the bladder lumen (Peterson, Goss & Atryzek 1974). Muscle strips from guinea pig bladders hypertrophied by this procedure have been found to develop less maximal active force than strips from untreated bladders.…”

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confidence: 93%

Length‐tension relations of smooth muscle from normal and denervated rat urinary bladders

Ekström

Uvelius

1981

Acta Physiologica Scandinavica

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Urinary bladders of rats were denervated by bilateral excision of the pelvic ganglion and removed 10 days after the operation. They were filled with 0.75 ml saline and a longitudinal muscle strip was marked out, measured and dissected out. Strips from normal bladders filled with the same volume were used as controls. Denervated bladders were 4-5 times heavier than control bladders. Muscle strips from denervated bladders showed, in contrast to controls, marked phasic spontaneous contractions which were unaffected by tetrodotoxin, indicating a myogenic origin. Active tension in response to AC stimulation was measured at different lengths. In relation to the in situ length (Lin situ) at 0.75 ml the denervated strips had to be stretched to much greater extent than controls in order to reach optimum length (L0) for force development. Furthermore, the denervated strips shortened less in relation to Lin situ than the controls. If active length-tension relations were expressed in relation to L0, the difference between denervated and control strips was abolished. Maximal active force was the same for denervated and control strips. Water content increased significantly in denervated bladders. The results suggest a remodelling of the smooth muscle structure in denervated bladders; the characteristics of the contractile machinery seem, however, to be unaltered.

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“…In the present study, it was investigated whether hypertrophy as such would sensitize the bladder to parasympathomimetics. The presence of a paraffin bolus innavesically, serving as space filler, has been shown to cause bladder distension and a marked increase in bladder weight due to thickening of the muscle layer (Peterson et al 1974). We have now examined the in vztro responses of such hypertrophied urinary bladders Correspondence : Dr Jorgen Ekstrom, Department of Physiology and Biophysics, University of Lund, Solvegatan 19, S-223 62 Lund, Sweden.…”

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Transient supersensitivity in the hypertrophied rat urinary bladder

Ekström

Malmberg

Wallin

1986

Acta Physiologica Scandinavica

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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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Hypertrophy of the rat urinary bladder following reduction of its functional volume

Cited by 19 publications

References 11 publications

Hypertrophy of visceral smooth muscle

Hypertrophy of visceral smooth muscle

Length‐tension relations of smooth muscle from normal and denervated rat urinary bladders

Transient supersensitivity in the hypertrophied rat urinary bladder

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