The abnormal mobilization of Ca^<2+> and K^+ in diabetic skeletal muscle membranes

糖尿病骨骼肌膜Ca^2和K^的异常动员

基本信息

批准号：
61571093
负责人：
KIMURA Ikuko
金额：
$ 1.47万
依托单位：
Toyama Medical & Pharmaceutical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1986
资助国家：
日本
起止时间：
1986 至 1987
项目状态：
已结题

项目摘要

In order to study the cause of supersensitivity for succinylcholine, a depolarizing blocker, and the relation to the increase in the activity of Ca^<2+>-dependent neutral protease, K^+- and Ca^<2+>-mobilization were investigated in diaphragm muscles of alloxan mice.1. Based on steady-state current-voltage (I - V) relationships, resting membrane conductance was decreased by diabetic state. Tetraethylammonium, a K^+channel blocker, and cesium chloride, a K^+ influx inhibitor, became less effective in diabetic state than in normal state. The extent of decrease in resting membrane conductance by C1^--free medium was much greater in diabetic state than in normal muscles.2. Ca^<2+>-dependent slow action potentials were significantly decreased in amplitude and duration by diabetic state. Fatique developed regardless of the presence of verapamil in contrast to the quicker development of fatigue in normal muscles in response to verapamil.3. By the technique of aeguorin luminescence, changes of … More intracellular Ca^<2+> release were compared between diabetic, non-diabetic denervated and normal muscles. By external Ca^<2+>-free solution, Ca^<2+> transient was easily decreased in normal muscles, whereas in diabeic muscles it was less affected and clearly decreased only when the muscles were previously injected with EGTA. The extent of the decreasing effect was not changed by EGTA pretreatment of denervated muscles. The caffeineinduced increase in Ca^<2+> transient was still observed even under the Ca^<2+>-free solution after EGTA pretreatment of normal muscles, whereas it was changed to decreasing effects after the short duration of increase in diabetic and non-diabetic denervated muscles.4. Trifluoperazine, a calmodulin antagonist, suppressed more potently Ca^<2+> transients in diabetic state than in normal state.These results suggest that diabetic state causes (1) K^+ conductance decrease, (2) Ca^<2+> influx decrease, (3) external Ca^<2+>-independent Ca^<2+> release, and (4) external Ca^<2+>-dependent Ca^<2+> release by caffeine. Less

为了研究琥珀酰胆碱超敏反应的原因，脱甲基胆碱以及与Ca^<2+> - 依赖性中性蛋白酶，K^+ - 和Ca^<2+> - 动员的关系的关系在Alloxan小鼠的diaphragm肌肉中研究了。基于稳态电流电压（I-V）关系，糖尿病状态降低了静止的膜电导。四乙基铵，一个K^+通道阻滞剂和氯化纤维（K^+）抑制剂在糖尿病状态下的有效性低于正常状态。 C1^的静息膜电导降低的程度 - 糖尿病态的游离培养基远大于正常肌肉2。 Ca^<2+> - 依赖性缓慢的动作电位在放大器和糖尿病状态下的持续时间显着降低。 Fatique无论存在于维拉帕米的存在如何，与响应于维拉帕米的正常肌肉中疲劳的更快发展相反。3。通过赋蛋白发光的技术，比较了糖尿病，非糖尿病性糖尿病和正常肌肉之间更细胞内Ca^<2+>释放的变化。通过外部Ca^<2+> - 游离溶液，在正常肌肉中很容易降低CA^<2+>瞬态，而在腹肌肌肉中，它受到的影响较小，并且仅当肌肉先前注射EGTA时才明显降低。 EGTA预处理被取代的肌肉没有改变效果的降低程度。即使在EGTA预处理正常肌肉后，咖啡因诱导的Ca^<2+>瞬态的增加，即使在Ca^<2+> - 游离溶液下，咖啡因诱导的溶液也会被观察到，而在糖尿病和非糖尿病性无抑制性肌肉的持续时间较短后，它被更改为降低效果。4。三氟吡嗪是一种钙调蛋白拮抗剂，在糖尿病状态下比正常状态下更可能更有潜在地抑制Ca^<2+>瞬态。这些结果表明糖尿病状态原因（1）K^+电导率下降，（2）Ca^<2+>逐Ca^<2+影响下降，（3）外部Ca^<2+> - 独立的Ca^<2+ - 独立ca^<2+ever-（4）和（4），（4）咖啡馆。较少的