Exercise training prevents Ca2+ dysregulation in coronary smooth muscle from diabetic dyslipidemic yucatan swine.
Exercise training prevents Ca2+ dysregulation in coronary smooth muscle from diabetic dyslipidemic yucatan swine.
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运动训练可防止糖尿病血脂异常尤卡坦猪冠状动脉平滑肌中的 Ca2+ 失调。
DOI：
10.1152/japplphysiol.00235.2006
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Sturek,Michael
中科院分区：
文献类型：
--
作者：
Witczak,CarolA;Wamhoff,BrianR;Sturek,Michael
众所周知，有氧运动训练在疾病中具有深远的心脏保护作用，但细胞机制仍未明确。我们检验了肌浆网Ca2+缓冲增加和电压门控Ca2+通道密度增加的假设，这是糖尿病血脂异常中冠状动脉平滑肌细胞内Ca2+(Ca2+i)失调的基础，运动训练可以防止这些增加。尤卡坦猪被维持在1)对照、2)四氧嘧啶诱导的高血糖、3)高脂肪/高胆固醇喂养、4)高血糖加高脂肪/高胆固醇喂养（糖尿病性血脂异常）和5)糖尿病性血脂异常加运动训练（跑步机跑步）的条件下。20周后，取心脏，从右冠状动脉分离平滑肌细胞。我们利用钙离子水平的fura-2成像来分离肌内质网Ca2+- atp酶（SERCA）与Na+-Ca2+交换器和质乳Ca2+- atp酶的功能作用，并利用全细胞膜片钳来检测电压门控Ca2+通道电流密度（即Ca2+内流）。结果表明，糖尿病性血脂异常损害了血浆Ca2+外流，增加了基础Ca2+ il水平，增加了SERCA蛋白和肌浆网Ca2+缓冲，并引起电压门控Ca2+通道电流密度降低了50%。运动训练与糖尿病血脂异常状态恢复浆体Ca2+外排、SERCA蛋白、肌浆网Ca2+缓冲和电压门控Ca2+通道电流密度到控制水平。有趣的是，与对照组相比，运动训练组的基础Ca2+水平显著降低。总的来说，这些结果证明了运动在预防糖尿病性血脂异常引起的Ca2+失调中的关键作用。
Aerobic exercise training is known to have profound cardioprotective effects in disease, yet cellular mechanisms remain largely undefined. We tested the hypothesis that increased sarcoplasmic reticulum Ca2+buffering and increased voltage-gated Ca2+channel density underlie coronary smooth muscle intracellular Ca2+(Ca2+i) dysregulation in diabetic dyslipidemia and that exercise training would prevent these increases. Yucatan swine were maintained in1) control,2) alloxan-induced hyperglycemic,3) high fat/cholesterol fed,4) hyperglycemic plus high fat/cholesterol fed (diabetic dyslipidemic), and5) diabetic dyslipidemic plus exercise-trained (treadmill running) conditions. After 20 wk, the heart was removed and smooth muscle cells isolated from the right coronary artery. We utilized fura-2 imaging of Ca2+ilevels to separate the functional role of the sarcoendoplasmic reticulum Ca2+-ATPase (SERCA) from the Na+-Ca2+exchanger and the plasmalemmal Ca2+-ATPase, and whole-cell patch clamp to examine voltage-gated Ca2+channel current density (i.e., Ca2+influx). Results indicated that diabetic dyslipidemia impaired plasmalemmal Ca2+efflux, increased basal Ca2+ilevels, increased SERCA protein and sarcoplasmic reticulum Ca2+ibuffering, and elicited an ∼50% decrease in voltage-gated Ca2+channel current density. Exercise training concurrent with the diabetic dyslipidemic state restored plasmalemmal Ca2+efflux, SERCA protein, sarcoplasmic reticulum Ca2+ibuffering, and voltage-gated Ca2+channel current density to control levels. Interestingly, basal Ca2+ilevels were significantly lower in the exercise-trained group compared with control. Collectively, these results demonstrate a crucial role for exercise in the prevention of diabetic dyslipidemia-induced Ca2+idysregulation.
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