Physiological fatigue of smooth muscle contractions in rat urinary bladder

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Abstract

OBJECTIVE

To characterize the physiological fatigue in bladder smooth muscles that can occur within 60 s of stimulation, which is closer to the duration of normal voiding.

MATERIALS AND METHODS

Longitudinal and transverse strips of rat bladder were used; the muscles were mounted in an in vitro multi-muscle chamber, and the decline in contractile tension recorded during continuous electrical stimulation at frequencies of 5–30 Hz for 60 s. The effect of muscle length on fatigue was assessed by monitoring the decline in tension during 30 Hz stimulation at rest length, and at 60% and 100% stretched lengths of the bladder strips. To assess some of the factors involved in the development of fatigue, tension responses of fatigued muscles were monitored on exposure to 80 mM potassium or 1 μM bethanechol.

RESULTS

In both longitudinal and transverse bladder strips stimulated at 30 Hz, peak contractile tension declined to 50% of original after ≈ 33 s, and to 30% after 60 s of stimulation. After 10 s rest, 60% of the original tension was recovered. Increasing the frequency of fatigue stimulation from 5 to 30 Hz significantly increased the extent of the decline in tension and reduced the time to a 50% decrease in tension. Stretching the bladder strips from rest length to 100% stretched length significantly reduced the extent of tension decline and increased the time to a 50% decrease in tension. Exposure of fatigued muscles to high potassium or bethanechol generated more tension than electrical stimulation.

CONCLUSION

Contractile fatigue occurs in both longitudinal and transverse strips of the bladder smooth muscles within the duration of normal voiding. Increasing the frequency of stimulation from 5 to 30 Hz increased the degree and rate of fatigue. Stretching the bladder strips from rest length by 60–100% reduced the degree and rate of fatigue. Bladder fatigue may be caused by decreased depolarization of the smooth muscle membranes, reduced release of acetylcholine from presynaptic nerve terminals, or by other yet undetermined mechanisms.

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