BACKGROUND Few studies examined the effect of long-acting nitrates on renal function in chronic heart failure (CHF). Thus, we aimed to investigate the effect of long-acting nitrate on the expression of adrenoceptors (AR) and angiotensin II receptor (ATR) subtypes of the renal cortex, in rats with myocardial infarction-induced CHF. METHODS Rats were randomly divided into the following groups: control, sham-operated, CHF, low- and high-dose nitrate, positive drug control (olmesartan), and high-dose of long-acting nitrate + olmesartan. Ultrasound echocardiography markers were compared, and the levels of AR subtypes, AT1R, and AT2R were measured using reverse transcription-polymerase chain reaction and western blot analysis. Histopathology of the kidney was determined on hematoxylin and eosin-stained sections. RESULTS CHF significantly increased plasma renin activity (PRA) and angiotensin II levels, upregulated AT1R expression and downregulated α1A-, β1-, β2-AR, and AT2R expression compared to the sham control. High-dose nitrate or olmesartan alone, and especially in combination, decreased the levels of PRA and angiotensin II and downregulated the CHF-induced expression of AT1R, α1A-, β1-, and β2-AR, and AT2R. CHF resulted in significant impairment of the renal tissue, including inflammatory cells infiltration to the tubular interstitium and surrounding the renal glomerulus, and tubular necrosis, which was alleviated in all treatment groups to different degrees. CONCLUSIONS Long-acting nitrates could reverse CHF-induced changes in AR and ATR subtypes in the kidney, and improve cardiac function to protect renal function. Compared with monotherapy, the combination of nitrates and olmesartan shows more significant benefits in regulating AR and ATR subtypes.

中文翻译：

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高剂量硝酸盐治疗可恢复心肌梗塞引起的心力衰竭大鼠肾皮质α1和β-肾上腺素受体亚型以及血管紧张素II受体的表达。

背景 很少有研究探讨长效硝酸盐对慢性心力衰竭（CHF）肾功能的影响。因此，我们的目的是研究长效硝酸酯对心肌梗塞诱发的 CHF 大鼠肾皮质肾上腺素受体 (AR) 和血管紧张素 II 受体 (ATR) 亚型表达的影响。方法将大鼠随机分为以下组：对照组、假手术组、CHF组、低剂量和高剂量硝酸酯组、阳性药物对照组（奥美沙坦）、高剂量长效硝酸酯+奥美沙坦组。比较超声心动图标记物，并使用逆转录聚合酶链反应和蛋白质印迹分析测量 AR 亚型、AT1R 和 AT2R 的水平。肾脏的组织病理学通过苏木精和伊红染色的切片来确定。结果与假手术对照相比，CHF 显着增加血浆肾素活性 (PRA) 和血管紧张素 II 水平，上调 AT1R 表达，下调 α1A-、β1-、β2-AR 和 AT2R 表达。单独使用高剂量硝酸盐或奥美沙坦，特别是联合使用，可降低 PRA 和血管紧张素 II 的水平，并下调 CHF 诱导的 AT1R、α1A-、β1-、β2-AR 和 AT2R 的表达。CHF导致肾组织明显受损，包括炎性细胞浸润至肾小管间质和肾小球周围，以及肾小管坏死，但各治疗组均有不同程度减轻。结论长效硝酸酯类药物可逆转CHF引起的肾脏AR和ATR亚型变化，改善心功能，保护肾功能。与单药治疗相比，硝酸酯类药物与奥美沙坦联合治疗在调节AR和ATR亚型方面显示出更显着的益处。