Effects of streptozotocin-induced diabetes mellitus on intracellular calcium and contraction of longitudinal smooth muscle from rat urinary bladder.

PURPOSE

To examine the effect of diabetes on [Ca2+]i and contractility in longitudinal smooth muscle of the urinary bladder.

MATERIALS AND METHODS

Longitudinal smooth muscle strips were isolated from the urinary bladders of rats with STZ-induced diabetes as well as age matched controls. Force and [Ca2+]i were measured simultaneously in muscle strips loaded with the calcium indicator, fura-2. Contractions were initiated by electrical field stimulation (EFS) at various frequencies, as well as by high K+, carbachol (CCh) and cyclopiazonic acid (CPA) in the presence of varying concentrations of extracellular Ca2+.

RESULTS

In unstimulated muscles, there was no significant difference in resting [Ca2+]i between the control and diabetic groups. However, the muscle strips from the diabetic animals produced higher force levels in response to EFS, high K+, CCh and CPA than those from control animals. The higher force development in the diabetic muscles was not associated with greater increases in [Ca2+]i, which in fact tended to be lower during stimulation in the diabetic tissues. When stimulated by CCh in the presence of nifedipine, both control and diabetic muscles exhibited a nifedipine-resistant component of contraction, however, this was significantly larger in the diabetic muscles.

CONCLUSION

The results suggest that there are no major impairments in either intracellular calcium regulation or contractile function in bladder smooth muscle after 8-weeks of STZ-induced diabetes. However, a non-specific enhancement of force production was seen, which was not associated with increases in [Ca2+]i. These changes imply that the apparent sensitivity to [Ca2+]i is enhanced in bladder smooth muscle from diabetic rats.