AIM The inward rectifier K+ (Kir) channels and prostanoids are important factors in regulating vascular tone, but the relationship between them has not been well studied. We aimed to study the involvement of prostanoids in regulating Kir activity in the rat intrarenal arteries (RIRAs). MAIN METHODS The vascular tone of isolated RIRAs was recorded with a wire myograph. The intracellular Ca2+ concentrations ([Ca2+]i) and Kir currents were measured with a Ca2+-sensitive fluorescence probe and patch clamp, respectively, in the arterial smooth muscle cell (ASMC) freshly isolated from RIRAs. Kir2.1 expression in RIRAs was assayed by Western blotting. KEY FINDINGS At 0.03-1.0 mM, BaCl2 (a specific Kir blocker) concentration-dependently contracted RIRAs and elevated [Ca2+]i levels. Mild stimulations with various vasoconstrictors at low concentrations significantly potentiated RIRA contraction induced by Kir closure with BaCl2. In both the quiescent and the stimulated RIRAs, cyclooxygenase inhibition and thromboxane-prostanoid receptor (TPR) antagonism depressed BaCl2-induced RIRA contraction, while nitric oxide (NO) synthetase inhibition and endothelium-denudation enhanced the contraction. Kir2.1 expression was significantly more abundant in smaller RIRAs. Ba2+-sensitive Kir currents were depressed by TPR agonist U46619 while increased by NO donor sodium nitroprusside. SIGNIFICANCE The present results reveal that vasoconstrictor stimulation augments RIRA contraction induced by Kir closure with Ba+ and indicate that prostanoid synthesis followed by TPR activation is involved in the modulation of the myocyte Kir activity. This study suggests that prostanoid synthesis and TPR may be potential targets for dysfunctions in renal blood circulation.

中文翻译：

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前列腺素有助于调节肾内动脉平滑肌细胞中向内整流的K +通道。

目的内向整流器K +（Kir）通道和前列腺素类是调节血管紧张度的重要因素，但它们之间的关系尚未得到很好的研究。我们旨在研究前列腺素类参与调节大鼠肾动脉（RIRA）中Kir活性的过程。主要方法用钢丝肌电图记录孤立的RIRA的血管张力。在刚从RIRA分离的动脉平滑肌细胞（ASMC）中，分别使用Ca2 +敏感的荧光探针和膜片钳测量细胞内Ca2 +浓度（[Ca2 +] i）和Kir电流。通过蛋白质印迹分析RIRA中的Kir2.1表达。主要发现在0.03-1.0 mM处，BaCl2（一种特定的Kir阻滞剂）浓度依赖性地使RIRA收缩并升高[Ca2 +] i水平。低浓度各种血管收缩剂的轻度刺激可显着增强BaCl2 Kir封闭诱导的RIRA收缩。在静态和刺激的RIRA中，环氧合酶抑制和血栓烷-前列腺素受体（TPR）拮抗作用均会抑制BaCl2诱导的RIRA收缩，而一氧化氮（NO）合成酶的抑制作用和内皮剥脱作用则增强了收缩。在较小的RIRA中，Kir2.1表达明显更为丰富。TPR激动剂U46619抑制了Ba2 +敏感的Kir电流，而NO供体硝普钠增加了Ba2 +敏感的Kir电流。意义本发明结果表明，血管收缩剂刺激增强了用Ba +封闭Kir所诱导的RIRA收缩，并表明前列腺素合成后TPR激活参与了肌细胞Kir活性的调节。