Isosmotic Contraction of Rat Aortic Smooth Muscle Cells upon Activation of Purinergic Receptors: the Role of Chlorine Transport

IF 0.6 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
L. V. Smaglii, V. S. Gusakova, S. V. Gusakova, M. A. Pshemyskiy, S. O. Koshuba, E. A. Golovanov
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引用次数: 0

Abstract

We studied the effect of the purinergic signaling system and the contribution of Cl transporters to isosmotic contraction of vascular smooth muscle cells (SMC), which results from the normalization of osmotic pressure after prolonged incubation in a hyposmotic medium. The study was carried out by myography of endothelium-denuded aortic ring segments of male Wistar rats. Isosmotic contraction was induced by placing vascular segments in normosmotic Krebs solution (120 mM NaCl) after a 40-minute incubation in a hyposmotic Krebs solution (40 mM NaCl). Purinergic receptors were activated by adenosine 5’-triphosphate (ATP, 500 µM), a nonselective P2X and P2Y receptor agonist, and uridine 5’-triphosphate (UTP, 500 µM), a selective P2Y receptor agonist. ATP and UTP abolished the transience of the aortic SMC isosmotic contraction without affecting its amplitude. Pretreatment of vascular segments with ATP and UTP during incubation in a hyposmotic solution completely suppressed the development of isosmotic contraction in the presence of ATP or UTP, but did not affect it without purinergic receptor activators. The Na+–K+–2Cl-cotransporter (NKCC) inhibitor bumetanide (100 µM) abolished isosmotic contraction in the presence of ATP (not UTP) but restored its transience. The nonselective Cl channel and Cl/HCO3 exchanger blocker DIDS (100 µM) suppressed the development of isosmotic contraction in the presence of both ATP and UTP. The potassium channel blocker tetraethylammonium (10 mM) potentiated the contractile activity of UTP toward isosmotic volume contraction. Presumably, purinergic receptors abolish the transience of isosmotic contraction by activating Cl currents through activation of P2Y receptors. The mechanism of interaction between the purinergic signaling system and Cl transport during cell volume changes requires further investigation.

Abstract Image

嘌呤能受体激活后大鼠主动脉平滑肌细胞的等渗收缩:氯转运的作用
摘要 我们研究了嘌呤能信号系统的作用以及Cl-转运体对血管平滑肌细胞(SMC)等渗收缩的贡献。这项研究是通过对雄性 Wistar 大鼠内皮剥离的主动脉环段进行肌电图检查而进行的。在低渗透性克雷布斯溶液(40 毫摩尔氯化钠)中培养 40 分钟后,将血管段置于正常渗透性克雷布斯溶液(120 毫摩尔氯化钠)中,可诱导等渗透性收缩。嘌呤能受体被 5'-triphosphate 腺苷(ATP,500 µM)(一种非选择性 P2X 和 P2Y 受体激动剂)和 5'-triphosphate 尿苷(UTP,500 µM)(一种选择性 P2Y 受体激动剂)激活。ATP 和UTP 可取消主动脉 SMC 等渗收缩的瞬时性,但不影响其幅度。Na+-K+-2Cl-共转运体(NKCC)抑制剂布美他尼(Bumetanide)(100 µM)在ATP(而非UTP)存在的情况下取消了等渗收缩,但恢复了其瞬时性。然后,选择性 Cl- 通道和 Cl-/HCO3- 交换阻断剂 DIDS(100 µM)抑制了在 ATP 和 UTP 存在下等渗收缩的发展。钾通道阻断剂四乙基铵(10 mM)增强了UTP对等渗体积收缩的收缩活性。据推测,嘌呤能受体通过激活P2Y受体来激活Cl-电流,从而取消了等渗收缩。细胞体积变化过程中嘌呤能信号系统与 Cl- 转运之间的相互作用机制有待进一步研究。
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来源期刊
自引率
33.30%
发文量
110
审稿时长
6-12 weeks
期刊介绍: Journal of Evolutionary Biochemistry and Physiology  publishes original experimental and theoretical and review articles related to evolution of the main forms of metabolism in connection with life origin; comparative and ontogenetic physiology and biochemistry, biochemical evolution of animal world; as well as evolution of functions; morphology, pharmacology, pathophysiology and ecological physiology. The journal welcomes manuscripts from all countries in the English or Russian language.
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