肾素-血管紧张素-醛固酮系统(RAAS)在维持体内各种生理过程中起着至关重要的作用,包括血压调节,电解质平衡,和整体心血管健康。然而,任何已知干扰RAAS的化合物或药物可能对跨膜离子电流有额外的影响。在这篇回顾性评论文章中,我们的目的是提供一系列长期被认为会干扰RAAS的化合物或药物.值得注意的是,这些物质还可以在不同类型的离子电流中表现出调节作用。Apocynin,已知减弱血管紧张素II诱导的上皮Na+通道的激活,显示出刺激电压门控Na电流(INa)的峰值和后期分量。依沙瑞酮,盐皮质激素受体的拮抗剂,可以直接对峰值和晚期INa产生抑制作用。地塞米松,合成糖皮质激素,可以直接提高大电导Ca2+激活K+通道的开放概率。Sparsentan,血管紧张素II受体和内皮素A型受体的双重作用拮抗剂,发现有效抑制峰值和晚期INa的幅度。然而,替米沙坦,血管紧张素II受体阻滞剂,有效刺激峰值和晚期INa,同时减慢电流的失活时间。然而,替米沙坦的存在也可以抑制erg介导的钾电流。此外,托伐普坦,被认为是一种可以阻断加压素受体的抗水性药物,注意到直接抑制延迟整流器K电流和M型K电流的幅度。以上结果表明,这些物质不仅对RAAS具有干扰作用,而且对不同类型的离子电流也具有调节作用。因此,为了确定他们的行动机制,有必要获得更深入的理解。
The renin-angiotensin-aldosterone system (RAAS) plays a crucial role in maintaining various physiological processes in the body, including blood pressure regulation, electrolyte balance, and overall cardiovascular health. However, any compounds or drugs known to perturb the RAAS might have an additional impact on transmembrane ionic currents. In this retrospective review article, we aimed to present a selection of chemical compounds or medications that have long been recognized as interfering with the RAAS. It is noteworthy that these substances may also exhibit regulatory effects in different types of ionic currents. Apocynin, known to attenuate the angiotensin II-induced activation of epithelial Na+ channels, was shown to stimulate peak and late components of voltage-gated Na+ current (INa). Esaxerenone, an antagonist of the mineralocorticoid receptor, can exert an inhibitory effect on peak and late INa directly. Dexamethasone, a synthetic glucocorticoid, can directly enhance the open probability of large-conductance Ca2+-activated K+ channels. Sparsentan, a dual-acting antagonist of the angiotensin II receptor and endothelin type A receptors, was found to suppress the amplitude of peak and late INa effectively. However, telmisartan, a blocker of the angiotensin II receptor, was effective in stimulating the peak and late INa along with a slowing of the inactivation time course of the current. However, telmisartan\'s presence can also suppress the erg-mediated K+ current. Moreover, tolvaptan, recognized as an aquaretic agent that can block the vasopressin receptor, was noted to suppress the amplitude of the delayed-rectifier K+ current and the M-type K+ current directly. The above results indicate that these substances not only have an interference effect on the RAAS but also exert regulatory effects on different types of ionic currents. Therefore, to determine their mechanisms of action, it is necessary to gain a deeper understanding.