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首页> 外文期刊>Life sciences >Increase in calcium responsiveness of cardiac myofilament activation in ovariectomized rats.
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Increase in calcium responsiveness of cardiac myofilament activation in ovariectomized rats.

机译：去卵巢大鼠心肌肌丝激活的钙反应性增加。

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To evaluate a possible role of ovarian sex hormones in the Ca2+ responsiveness of cardiac myofilament activation, the relations of pCa (-log Ca2+ molar concentration) to actomyosin adenosine triphosphatase (ATPase) activity of isolated myofibrillar preparations from 8-10 week ovariectomized (Ovx) rat hearts were compared with those from sham-operated hearts. Deficiency of ovarian sex hormones in plasma of ovariectomized rats was indirectly verified by a significant reduction in uterine weights. Body weights of the ovariectomized rats were significantly greater than those of sham-operated controls. Despite a significant increase in heart weight of 10 week ovariectomized animals, the percent of heart weight-to-body weight ratio was not different from control group. The maximum myofibrillar ATPase activity at pH 7.0 was significantly suppressed after ovariectomy in both eight and ten week groups. However, the maximum ATPase activity at pH 6.5 was significantly suppressed only in 10 week ovariectomized hearts. Surprisingly, in every condition with depressed maximum myofibrillar ATPase activity, the pCa-actomyosin ATPase relationships of ovariectomized cardiac myofilaments demonstrated a significant leftward shift in pCa50 (-log half-maximally Ca2+ activation) from those of sham-operated controls. There was, however, no change in the Hill-coefficient of these cardiac myofilaments after ovariectomy. Analysis of myofilament proteins using gel electrophoresis demonstrated neither change nor loss of any thin filament proteins. These results indicate a possible modulating effect of ovarian sex hormone deficiency on the Ca2+ responsiveness of cardiac myofilament activation by induction of myofilament Ca2+ hypersensitivity but suppression of maximum myofibrillar ATPase activity.
机译：为了评估卵巢性激素在心肌肌丝活化的Ca2 +反应性中的可能作用，pCa（-log Ca2 +摩尔浓度）与离体8-10周去卵巢（Ovx）的分离的肌原纤维制剂肌动蛋白腺苷三磷酸酶（ATPase）活性的关系将大鼠心脏与假手术心脏进行比较。卵巢重量显着降低间接证实了卵巢切除大鼠血浆中卵巢性激素的缺乏。去卵巢大鼠的体重明显大于假手术对照组的体重。尽管10周去卵巢动物的心脏重量显着增加，但心脏重量与体重的百分比与对照组没有差异。在八周和十周组的卵巢切除术后，pH 7.0时最大的肌原纤维ATPase活性被显着抑制。但是，仅在10周去卵巢的心脏中，pH 6.5时的最大ATPase活性被显着抑制。出乎意料的是，在每种情况下，最大肌原纤维ATPase活性降低，卵巢切除的心肌细丝的pCa-肌球蛋白ATPase关系显示，与假手术对照组相比，pCa50明显向左移动（最大半数Ca2 +的对数对数）。然而，卵巢切除后这些心肌肌丝的希尔系数没有变化。使用凝胶电泳对肌丝蛋白进行分析表明，任何细丝蛋白均无变化或丢失。这些结果表明卵巢性激素缺乏可能通过诱导肌丝Ca2 +超敏反应但抑制最大的肌原纤维ATPase活性来调节心肌肌丝激活的Ca2 +反应性。

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