Salt Hypertension(盐高血压)研究综述
Salt Hypertension 盐高血压 - In this study, we generated ribosomal‐depleted RNA sequencing data from normal mouse kidneys and from injured mouse kidneys induced by deoxycorticosterone acetate‐salt hypertension and identified at least 4900 circRNA candidates. [1] Together, these results support that activation of PRR contributes to increased excitability and firing discharge of MNNs and increased plasma levels of VP in DOCA-salt hypertension. [2] Abcc6 loss-of-function is associated with greater cardiovascular calcification and fibrosis in mice subjected to DOCA-Salt hypertension. [3] NEW & NOTEWORTHY PRR knockdown in PVN neurons attenuates the development of DOCA-salt hypertension and autonomic dysfunction through a decrease in ERK1/2 activation in the PVN and RVLM during hypertension. [4] In a different set of 14-day Ang II-salt-treated rats, mini-osmotic pumps were used to infuse either a nonselective COX (cyclooxygenase) inhibitor ketorolac, L-PGDS inhibitor AT56, or DP1R inhibitor BWA868C to test the role of brain COX-PGD2-DP1R signaling in Ang II-salt hypertension. [5] DOCA-salt hypertension was induced by DOCA (20 mg/kg s. [6] In the present study, the renal-protective effect of hawthorn fruit extract (HW) on high-salt hypertension and its effect on metabolic patterns are determined. [7] KO of Dusp5 enhanced the myogenic tone of the renal afferent arteriole and interlobular artery in vitro with or without induction of deoxycorticosterone acetate-salt hypertension. [8] Methods— Aneurysms were induced by a single stereotaxic injection of elastase into the cerebrospinal fluid at the skull base, combined with systemic deoxycorticosterone-salt hypertension, without or with high-salt diet, for mild or severe outcomes, respectively. [9] The aim of our study was to establish the morphodensitometric features of locus coeruleus (LC) neurons nuclei in the brain stem of rats with arterial hypertension of various origin (essential – SHR and endocrine-salt hypertension (ESH)). [10]在这项研究中，我们从正常小鼠肾脏和由醋酸脱氧皮质酮 - 盐高血压诱导的受损小鼠肾脏生成了核糖体耗尽的 RNA 测序数据，并确定了至少 4900 个候选 circRNA。 [1] 总之，这些结果支持 PRR 的激活有助于增加 MNN 的兴奋性和放电放电，并增加 DOCA 盐高血压中 VP 的血浆水平。 [2] Abcc6 功能丧失与 DOCA-Salt 高血压小鼠的心血管钙化和纤维化程度更高有关。 [3] PVN 神经元中新的和值得注意的 PRR 敲低通过降低高血压期间 PVN 和 RVLM 中的 ERK1/2 激活来减轻 DOCA 盐高血压和自主神经功能障碍的发展。 [4] 在一组不同的 14 天 Ang II 盐处理的大鼠中，使用微型渗透泵来输注非选择性 COX（环氧合酶）抑制剂酮咯酸、L-PGDS 抑制剂 AT56 或 DP1R 抑制剂 BWA868C，以测试大脑的作用Ang II-盐高血压中的 COX-PGD2-DP1R 信号传导。 [5] DOCA (20 mg/kg s. [6] 在本研究中，确定了山楂果提取物 (HW) 对高盐高血压的肾脏保护作用及其对代谢模式的影响。 [7] Dusp5 的 KO 增强了体外肾传入小动脉和小叶间动脉的肌源性张力，无论是否诱导醋酸脱氧皮质酮 - 盐高血压。 [8] 方法——通过将弹性蛋白酶单次立体定向注射到颅底的脑脊液中，并结合全身性脱氧皮质酮-盐高血压，不伴或伴高盐饮食，分别针对轻度或重度结果诱导动脉瘤。 [9] 我们研究的目的是确定患有各种来源的动脉高血压（必需 - SHR 和内分泌盐高血压 (ESH)）大鼠脑干中蓝斑 (LC) 神经元核的形态密度测量特征。 [10]