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.