Pressure induces intracellular calcium changes in juxtaglomerular cells in perfused afferent arterioles.
Pressure induces intracellular calcium changes in juxtaglomerular cells in perfused afferent arterioles.
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DOI：
10.1038/hr.2011.65
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发表时间：
2011-08
期刊：
影响因子：
--
通讯作者：
Liu R
中科院分区：
文献类型：
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作者：
Lai EY;Wang Y;Persson AE;Manning RD Jr;Liu R
钙(Ca~(2+))在几乎所有类型的细胞分泌中都扮演着重要的角色，尤其是在肾脏的肾小球旁(JG)细胞中扮演着特别新的角色。在JG细胞中，钙离子抑制肾素的分泌，肾素是血压和肾脏血流动力学的主要调节因素。然而，传入小动脉(Af-Art)压力的改变是否会改变JG细胞内的钙离子浓度([Ca~(2+)]_i)，以及[Ca~(2+)]_i是来自细胞外还是细胞内，目前尚不清楚。我们假设Af-Art中灌流压力的增加导致JG细胞内[Ca~(2+)]i的升高。我们分离和灌流了C57BL6小鼠的Af-Art，并测定了JG细胞内[Ca~(2+)]i随灌流压力变化的变化。在60 mm Hg灌流压力下，JG细胞[Ca~(2+)]i为93·3±2·2 nm，在80、10 0、120、140 mm Hg时分别增加到111.3±13·4、119.6±7·3、130.3±2·9和140.8±12·1 nm。在12 0毫米汞柱下，机械敏感型阳离子通道阻滞剂Gd(94 6±7 5 nm)、L类钙通道阻滞剂硝苯地平(105.8±7 5 nm)、无钙溶液加乙二醇四乙酸(96 0±5 8 nm)均可降低小鼠心肌细胞[Ca~(2+)]i升高。同时，磷脂酶C抑制剂、三磷酸肌醇受体抑制剂、T型钙通道阻滞剂、N型钙通道阻滞剂和钙-三磷酸腺苷酶抑制剂对JG细胞[Ca~(2+)]_i的变化无明显影响。综上所述，JG细胞[Ca~(2+)]i随着灌流压力的升高而升高；此外，钙离子来源于细胞外，特别是机械敏感的阳离子通道和L型钙通道。
Calcium (Ca2+) has an important role in nearly all types of cellular secretion, with a particularly novel role in the juxtaglomerular (JG) cells in the kidney. In JG cells, Ca2+ inhibits renin secretion, which is a major regulator of blood pressure and renal hemodynamics. However, whether alterations in afferent arteriolar (Af-Art) pressure change intracellular Ca2+ concentration ([Ca2+]i) in JG cells and whether [Ca2+]i comes from extracellular or intracellular sources remains unknown. We hypothesize that increases in perfusion pressure in the Af-Art result in elevations in [Ca2+]i in JG cells. We isolated and perfused Af-Art of C57BL6 mice and measured changes in [Ca2+]i in JG cells in response to perfusion pressure changes. The JG cells’ [Ca2+]i was 93.3 ± 2.2 nm at 60 mm Hg perfusion pressure and increased to 111.3 ± 13.4, 119.6 ± 7.3, 130.3 ± 2.9 and 140.8 ± 12.1 nm at 80, 100, 120 and 140 mm Hg, respectively. At 120 mm Hg, increases in [Ca2+]i were reduced in mice receiving the following treatments: (1) the mechanosensitive cation channel blocker, gadolinium (94.6 ± 7.5 nm); (2) L-type calcium channel blocker, nifedipine (105.8 ± 7.5 nm); and (3) calcium-free solution plus ethylene glycol tetraacetic acid (96.0 ± 5.8 nm). Meanwhile, the phospholipase C inhibitor, inositol triphosphate receptor inhibitor, T-type calcium channel blocker, N-type calcium channel blocker and Ca2+-ATPase inhibitor did not influence changes in [Ca2+]i in JG cells. In summary, JG cell [Ca2+]i rise as perfusion pressure increases; furthermore, the calcium comes from extracellular sources, specifically mechanosensitive cation channels and L-type calcium channels.