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首页> 外文期刊>Life sciences >INTRACELLULAR ALKALINIZATION BY NH4CL INCREASES CYTOSOLIC CA2+ LEVEL AND TENSION IN THE RAT AORTIC SMOOTH MUSCLE
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INTRACELLULAR ALKALINIZATION BY NH4CL INCREASES CYTOSOLIC CA2+ LEVEL AND TENSION IN THE RAT AORTIC SMOOTH MUSCLE

机译：NH4CL胞内碱化增加大鼠主动脉平滑肌细胞胞质CA2 +水平和张力

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摘要

Intracellular pH (pHi) is elucidated to be an important regulator of various cell functions, but the role of pHi in smooth muscle contraction remains to be clarified. The purpose of the present study is to examine the effects of cell alkalinization by exposure to NH4Cl on cytosolic Ca2+ level ([Ca2+]i) and on muscle tone. We attempted simultaneous measurements of both [Ca2+]i and contractile force in rat isolated thoracic aorta from which the endothelium was removed. NH4Cl (10 - 80 mM) increased both [Ca2+]i and muscle tone in the presence of external Ca2+. These responses were reproducible. The removal of Ca2+ from the nutrient solution partially inhibited the rise in [Ca2+]i and the smooth muscle contraction induced by NH4Cl. In addition, the Ca2+ channel blocker verapamil also partially attenuated the responses to NH4Cl. The NH4Cl-induced responses were gradually reduced as NH4Cl was repeatedly added in a Ca2+-free solution. Norepinephrine (NE, 1 mu M) induced a transient increase in [Ca2+]i and sustained contraction in the absence of external Ca2+, and the subsequent application of NE had little effect on [Ca2+]i. After internal Ca2+ stores were depleted by exposure to NE, the subsequent application of NH4Cl induced increases in [Ca2+]i and tension of the aorta in a Ca2+ free solution. These results suggest that NH4Cl mainly evokes Ca2+ release from the internal Ca2+ stores that are not linked with adrenergic ex-receptor and causes Ca2+ influx through voltage-dependent Ca2+ channels in the vascular smooth muscle. [References: 33]
机译：阐明细胞内pH（pHi）是各种细胞功能的重要调节剂，但pHi在平滑肌收缩中的作用仍有待阐明。本研究的目的是通过暴露于NH4Cl来检查细胞碱化对胞质Ca2 +水平（[Ca2 +] i）和肌肉张力的影响。我们试图同时测量大鼠离体的胸主动脉中[Ca2 +] i和收缩力，并从中去除内皮。在存在外部Ca2 +的情况下，NH4Cl（10-80 mM）会增加[Ca2 +] i和肌肉张力。这些反应是可重复的。从营养液中去除Ca2 +会部分抑制[Ca2 +] i的升高和由NH4Cl引起的平滑肌收缩。此外，Ca2 +通道阻滞剂维拉帕米也部分减弱了对NH4Cl的反应。随着将NH4Cl反复添加到不含Ca2 +的溶液中，NH4Cl诱导的响应逐渐降低。去甲肾上腺素（NE，1μM）诱导[Ca2 +] i短暂增加并在没有外部Ca2 +的情况下持续收缩，随后应用NE对[Ca2 +] i几乎没有影响。通过暴露于NE耗尽内部Ca2 +储存库后，随后使用NH4Cl可以诱导[Ca2 +] i和主动脉在无Ca2 +溶液中的张力增加。这些结果表明，NH4Cl主要引起内部Ca2 +存储中的Ca2 +释放，而这些内部Ca2 +存储与肾上腺素能受体无关，并通过血管平滑肌中的电压依赖性Ca2 +通道引起Ca2 +流入。 [参考：33]

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