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Increased calcium/magnesium ratio in SHR versus WKY of different ages

机译:不同年龄的SHR与WKY中钙镁比增加

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Alterations in the metabolism of calcium and magnesium have been implicated in the pathogenesis of primary hypertension. Calcium influx across the external cellular membrane in smooth muscle cells and cardiomyocytes plays a crucial role in the control of cellular excitation contraction and impulse propagation. Intracellular calcium and magnesium concentrations are controlled by reversible binding to specific calcium binding proteins. The calcium and magnesium flux across the external membrane is regulated by a calcium pump (calcium-magnesium-ATPase), calcium channels and binding to the membrane. In cell membranes and in lymphocytes of essential hypertensives our group showed increased calcium and a decreased magnesium and increased calcium/magnesium ratio in hypertensive cells. In this context, in aortic smooth muscle cells from 13 spontaneously hypertensive rats (SHR) of the Muenster strain (systolic blood pressure 188.4 +/- 9.8 mmHg) and 13 normotensive rats (NT, systolic blood pressure 118.5 +/- 7.2 mmHg) aged 9 months, the intracellular calcium and magnesium contents were measured under nearly in-vivo conditions by electron-probe microanalysis. Measurements were performed in aortic cryosections 3 μm thick. The calcium content was 124.7 +/- 4.5~* mmol/kg dry weight in SHR versus 110.3 +/- 4.1 mmol/kg dry weight in NT (Means +/- SD, p < 0.01), the magnesium content was 35.5 +/- 3.9~* in SHR versus 50.1 +/- 4.9 mmol/kg dry weight in NT/p < 0.01). The calcium/magnesium ratio was significantly increased in SHR versus NT (3.56 +/-0.39~* versus 2.23 +/- 0.27, p < 0.01). In hypertensive one month old animals the increase in the calcium/magnesium ratio was not as pronounced as in 9 months old animals. The calcium/magnesium ratio was measured 3.3 +/- 0.42 in SHR (n=8) as compared to 2.51 +/- 0.39 in normotensive animals (n=8, p < 0.01). Aortic smooth muscle cells from SHR are characterized by a markedly elevated intracellular calcium and decreased intracellular magnesium contents compared with normotensive cells. Cellular calcium and magnesium handling is disturbed in SHR aortic smooth muscle cells as it is in hypertensive blood cells. The increased calcium/magnesium ratio in hypertensive cells is a pathogenetic factor for the development of arteriosclerosis and hypertension.
机译:钙和镁代谢的改变与原发性高血压的发病机制有关。钙流入平滑肌细胞和心肌细胞的外部细胞膜,在控制细胞兴奋收缩和冲动传播中起着至关重要的作用。细胞内钙和镁的浓度是通过与特定钙结合蛋白的可逆结合来控制的。穿过外膜的钙和镁通量由钙泵(钙-镁-ATPase),钙通道和与膜的结合来调节。在原发性高血压的细胞膜和淋巴细胞中,我们的小组显示高血压细胞中钙增加,镁减少,钙/镁比增加。在这种情况下,来自13名Muenster应变自发性高血压大鼠(SHR)的主动脉平滑肌细胞(收缩压为188.4 +/- 9.8 mmHg)和13例血压正常的大鼠(NT,收缩压为118.5 +/- 7.2 mmHg) 9个月后,通过电子探针显微分析在几乎体内条件下测量细胞内钙和镁含量。在3μm厚的主动脉冰冻切片中进行测量。 SHR中的钙含量为124.7 +/- 4.5〜* mmol / kg干重,而NT中的钙含量为110.3 +/- 4.1 mmol / kg干重(均值+/- SD,p <0.01),镁含量为35.5 + / -SHR中为3.9〜*,而NT / p中的干重为50.1 +/- 4.9 mmol / kg(<0.01)。相对于NT,SHR中的钙镁比显着增加(3.56 +/- 0.39〜*对2.23 +/- 0.27,p <0.01)。在高血压一个月大的动物中,钙/镁比的增加不如在九个月大的动物中明显。在SHR(n = 8)中测得的钙/镁比为3.3 +/- 0.42,而在降压动物中则为2.51 +/- 0.39(n = 8,p <0.01)。与正常血压的细胞相比,来自SHR的主动脉平滑肌细胞的特征在于其细胞内钙含量明显升高,而细胞内镁含量却降低。 SHR主动脉平滑肌细胞中的钙离子和镁离子处理受到干扰,就像高血压血细胞中一样。高血压细胞中钙镁比的增加是动脉硬化和高血压发展的致病因素。

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