The aim of this study is to verify the impact of Leptin in blood pressure (BP) regulation and Leptin-resistance in metabolic/neurogenic hypertension through baroreflex afferents and dysregulation. Artery BP/heart rate (HR) were measured while nodose (NG) microinjection of Leptin, membrane depolarization/inward current were obtained by whole-cell patch from NG neurons isolated from adult female rats. Baroreflex sensitivity (BRS) tested with PE/SNP, distribution/expression of Leptin/receptors in the NG/nucleus tractus solitary (NTS) examined using immumostaining and qRT-PCR, and serum concentrations of Leptin/NE measured by ELISA were observed in control and high fructose-drinking induced hypertension (HTN-HFD) rats. The results showed that BP was significantly/dose-dependently reduced by Leptin NG microinjection likely through direct excitation of female-specific subpopulation of Ah-type neurons showing a potent membrane depolarization/inward currents. Sex-specific distribution/expression of OB-Ra/OB-Rb in the NG were detected with estrogen-dependent manner, similar observations were also confirmed in the NTS. As expected, BRS was dramatically decreased in the presence of PE/SNP in both male and female rats except for the female with PE at given concentrations. Additionally, serum concentration of Leptin was elevated in HFD-HTN model rats of either sex with more obvious in females. Under hypertensive condition, the mean fluorescent density of OB-R and mRNA expression for OB-Ra/OB-Rb in the NG/NTS were significantly down-regulated. These results have demonstrated that Leptin play a role in dominant parasympathetic drive via baroreflex afferent activation to buffer Leptin-mediated sympathetic activation systemically and Leptin-resistance is an innegligible mechanism for metabolic/neurogenic hypertension through baroreflex afferent dysregulation.

中文翻译：

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压力反射传入功能是了解瘦素介导的血压降低和瘦素抵抗性高血压的一部分

本研究的目的是通过压力反射传入和失调来验证瘦素对血压 (BP) 调节和瘦素抵抗对代谢性/神经源性高血压的影响。测量动脉血压/心率（HR），同​​时通过结节（NG）显微注射瘦素，通过从成年雌性大鼠分离的NG神经元的全细胞贴片获得膜去极化/内向电流。使用 PE/SNP 测试压力反射敏感性 (BRS)，使用免疫染色和 qRT-PCR 检查瘦素/孤立核束 (NTS) 中瘦素/受体的分布/表达，并在对照中观察通过 ELISA 测量的瘦素/NE 血清浓度和高果糖饮用诱发高血压（HTN-HFD）大鼠。结果表明，瘦素 NG 显微注射可显着/剂量依赖性地降低血压，这可能是通过直接激发女性特异性 Ah 型神经元亚群而表现出有效的膜去极化/内向电流。以雌激素依赖性方式检测NG中OB-Ra/OB-Rb的性别特异性分布/表达，在NTS中也证实了类似的观察结果。正如预期的那样，在给定浓度的 PE/SNP 存在下，雄性和雌性大鼠中的 BRS 均显着降低（雌性大鼠除外）。此外，HFD-HTN模型大鼠血清瘦素浓度升高，雌性更明显。在高血压条件下，NG/NTS中OB-R的平均荧光密度和OB-Ra/OB-Rb的mRNA表达显着下调。这些结果表明，瘦素通过压力反射传入激活在主导副交感神经驱动中发挥作用，以系统地缓冲瘦素介导的交感神经激活，并且瘦素抵抗是通过压力反射传入失调导致代谢/神经源性高血压的不可忽视的机制。