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首页> 外文期刊>Cardiovascular toxicology >Salusin beta Within the Nucleus Tractus Solitarii Suppresses Blood Pressure Via Inhibiting the Activities of Presympathetic Neurons in the Rostral Ventrolateral Medulla in Spontaneously Hypertensive Rats
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Salusin beta Within the Nucleus Tractus Solitarii Suppresses Blood Pressure Via Inhibiting the Activities of Presympathetic Neurons in the Rostral Ventrolateral Medulla in Spontaneously Hypertensive Rats

机译:Solutarii核内的Salusinβ通过抑制自发性高血压大鼠延髓前额叶延髓中交感神经元的活动来抑制血压

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摘要

Salusin beta is a newly identified bioactive peptide, which shows peripheral hypotensive, mitogenic and proatherosclerotic effects. The present study was undertaken to investigate the role of salusin beta within the nucleus tractus solitarii (NTS) and the underlying mechanism in regulating blood pressure and heart rate (HR) in spontaneously hypertensive rats (SHR). Our results showed that bilateral or unilateral microinjection of salusin beta (0.4-40 pmol) into the NTS in SHR decreased mean arterial pressure and HR in a dose-dependent manner. Bilateral microinjection of salusin beta (4 pmol) within NTS improved baroreflex sensitivity functions in SHR. Pretreatment with glutamate receptors antagonist kynurenic acid (5 nmol) into the NTS in SHR did not alter the salusin beta (4 pmol) induced hypotension and bradycardia. Likewise, bilateral vagotomy also did not alter the salusin beta (4 pmol) induced hypotension and bradycardia. However, pretreatment with GABA(A) receptors agonist muscimol (100 pmol) within the rostral ventrolateral medulla (RVLM) in SHR almost completely abolished the hypotension and bradycardia evoked by intra-NTS salusin beta (4 pmol). Our findings suggested that microinjection of salusin beta into the NTS produced hypotension and bradycardia, as well as improved baroreflex sensitivity functions, via inhibiting the activities of presympathetic neurons in the RVLM in SHR.
机译:Salusinβ是一种新近鉴定出的生物活性肽,具有外周降压,促有丝分裂和动脉粥样硬化作用。本研究旨在研究自发性高血压大鼠(SHR)孤束核(NTS)中salusinβ的作用以及调节血压和心率(HR)的潜在机制。我们的研究结果表明,SHR的NTS双向或单侧微量注射salusin beta(0.4-40 pmol)可降低平均动脉压和HR,且呈剂量依赖性。 NTS内双侧注射salusin beta(4 pmol)改善了SHR中的压力反射敏感性功能。在SHR中用谷氨酸受体拮抗剂强尿酸(5 nmol)预处理进入NTS不会改变salusin beta(4 pmol)引起的低血压和心动过缓。同样,双侧迷走神经切断术也没有改变salusin beta(4 pmol)引起的低血压和心动过缓。然而,在SHR的腹侧腹侧延髓(RVLM)中用GABA(A)受体激动剂麝香酚(100 pmol)进行的预处理几乎完全消除了NTS内salusin beta(4 pmol)引起的低血压和心动过缓。我们的发现表明,通过抑制SHR中RVLM中的交感神经元的活性,向NTS中微量注射salusinβ会产生低血压和心动过缓,并改善压力反射敏感性功能。

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