Neuropeptide Y (NPY), a metabolism-related cardiovascular factor, plays a crucial role in blood pressure (BP) regulation via peripheral and central pathways. The expression of NPY receptors (Y₁R/Y₂R) specific to baroreflex afferents impacts on the sexually dimorphic neural control of circulation. This study was designed to investigate the expression profiles of NPY receptors in the nodose ganglion (NG) and nucleus tractus solitary (NTS) under hypertensive conditions. To this end, rats with hypertension induced by N^G-nitro-L-arginine methylester (L-NAME) or high fructose drinking (HFD), and spontaneously hypertensive rats (SHRs) were used to explore the effects/mechanisms of NPY on BP using functional, molecular, and electrophysiological approaches. The data showed that BP was elevated along with baroreceptor sensitivity dysfunction in model rats; Y₁R was up- or down-regulated in the NG or NTS of male and female HFD/L-NAME groups, while Y₂R was only down-regulated in the HFD groups as well as in the NG of the male L-NAME group. In SHRs, Y₁R and Y₂R were both down-regulated in the NTS, and not in the NG. In addition to NPY-mediated energy homeostasis, leptin-melanocortin activation may be essential for metabolic disturbance-related hypertension. We found that leptin and α-melanocyte stimulating hormone (α-MSH) receptors were aberrantly down-regulated in HFD rats. In addition, α-MSH concentrations were reduced and NPY concentrations were elevated in the serum and NTS at 60 and 90 min after acute leptin infusion. Electrophysiological recordings showed that the decay time-constant and area under the curve of excitatory post-synaptic currents were decreased by Y₁R activation in A-types, whereas, both were increased by Y₂R activation in Ah- or C-types. These results demonstrate that sex- and afferent-specific NPY receptor expression in the baroreflex afferent pathway is likely to be a novel target for the clinical management of metabolism-related and essential hypertension.

中文翻译：

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Baroreflex传入途径对NPY介导的大鼠血压调节的贡献。

神经肽Y（NPY）是一种与代谢相关的心血管因子，在通过外周和中枢途径调节血压（BP）中起着至关重要的作用。压力反射传入神经特异的NPY受体（Y ₁ R / Y ₂ R）的表达影响循环的性双态神经控制。这项研究旨在调查在高血压情况下结节神经节（NG）和孤立性核束（NPS）中NPY受体的表达情况。为此，大鼠高血压诱导Ñ ^ģ-硝基-L-精氨酸甲酯（L-NAME）或高果糖饮用量（HFD）和自发性高血压大鼠（SHRs）使用功能，分子和电生理方法探讨了NPY对BP的影响/机制。数据显示，模型大鼠的血压升高并伴有压力感受器敏感性功能障碍。Y ₁ R在男性和女性HFD / L-NAME组的NG或NTS中被上调或下调，而Y ₂ R仅在HFD组以及男性L-FD的NG中被下调。 NAME群组。在SHR中，Y ₁ R和Y ₂R在NTS中均被下调，而在NG中均未下调。除了NPY介导的能量动态平衡外，瘦素-黑皮质素激活对于代谢紊乱相关性高血压也可能是必不可少的。我们发现瘦素和α-黑素细胞刺激激素（α-MSH）受体在HFD大鼠中异常下调。此外，急性瘦素输注后60和90分钟，血清和NTS中的α-MSH浓度降低，NPY浓度升高。电生理记录表明兴奋性突触后电流的曲线下的衰减时间常数和面积减少由Y ₁中A-类型的R活化，而，两者都增加了ÿ ₂R激活为Ah型或C型。这些结果表明，压力反射传入途径中的性别和传入特异性NPY受体表达可能是代谢相关和原发性高血压临床管理的新目标。