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链脲佐菌素诱导的糖尿病对大鼠膀胱纵行平滑肌细胞内钙及收缩功能的影响。

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

作者信息

Waring J V, Wendt I R

机构信息

Department of Physiology, Monash University, Clayton, Victoria, Australia.

出版信息

J Urol. 2000 Jan;163(1):323-30.

PMID:10604384
Abstract

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.

摘要

目的

研究糖尿病对膀胱纵行平滑肌细胞内钙离子浓度([Ca2+]i)及收缩性的影响。

材料与方法

从链脲佐菌素(STZ)诱导的糖尿病大鼠及年龄匹配的对照大鼠的膀胱中分离出纵行平滑肌条。在加载钙指示剂fura-2的肌肉条中同时测量张力和[Ca2+]i。通过不同频率的电场刺激(EFS)以及在不同细胞外Ca2+浓度存在下的高钾、卡巴胆碱(CCh)和环匹阿尼酸(CPA)引发收缩。

结果

在未受刺激的肌肉中,对照组和糖尿病组的静息[Ca2+]i无显著差异。然而,糖尿病动物的肌肉条对EFS、高钾、CCh和CPA的反应产生的张力水平高于对照动物。糖尿病肌肉中较高的张力发展与[Ca2+]i的更大增加无关,事实上在糖尿病组织刺激期间[Ca2+]i往往更低。当在硝苯地平存在下由CCh刺激时,对照和糖尿病肌肉均表现出硝苯地平抵抗性收缩成分,然而,这在糖尿病肌肉中显著更大。

结论

结果表明,在STZ诱导的糖尿病8周后,膀胱平滑肌的细胞内钙调节或收缩功能均无重大损害。然而,观察到了力量产生的非特异性增强,这与[Ca2+]i的增加无关。这些变化意味着糖尿病大鼠膀胱平滑肌对[Ca2+]i的明显敏感性增强。

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