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Oxytocin differently regulates pressor responses to stress in WKY and SHR rats: the role of central oxytocin and V1a receptors

机译:催产素不同地调节WKY和SHR大鼠对压力的升压反应:中央催产素和V1a受体的作用

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The role of central oxytocin in the regulation of cardiovascular parameters under resting conditions and during acute stress was investigated in male normotensive Wistar-Kyoto (WKY; n = 40) and spontaneously hypertensive rats (SHR; n = 28). In Experiment 1, mean arterial blood pressure (MABP) and heart rate (HR) were recorded in WKY and SHR rats at rest and after an air-jet stressor during intracerebroventricular (ICV) infusions of vehicle, oxytocin or oxytocin receptor (OTR) antagonist. In Experiment 2, the effects of vehicle, oxytocin and OTR antagonist were determined in WKY rats after prior administration of a V1a vasopressin receptor (V1aR) antagonist. Resting MABP and HR were not affected by any of the ICV infusions either in WKY or in SHR rats. In control experiments (vehicle), the pressor response to stress was significantly higher in SHR. Oxytocin enhanced the pressor response to stress in the WKY rats but reduced it in SHR. During V1aR blockade, oxytocin infusion entirely abolished the pressor response to stress in WKY rats. Combined blockade of V1aR and OTR elicited a significantly greater MABP response to stress than infusion of V1a antagonist and vehicle. This study reveals significant differences in the regulation of blood pressure in WKY and SHR rats during alarming stress. Specifically, the augmentation of the pressor response to stress by exogenous oxytocin in WKY rats is caused by its interaction with V1aR, and endogenous oxytocin regulates the magnitude of the pressor response to stress in WKY rats by simultaneous interaction with OTR and V1aR.
机译:在雄性正常血压Wistar-Kyoto(WKY; n = 40)和自发性高血压大鼠(SHR; n = 28)中研究了中央催产素在静息条件下和急性应激期间调节心血管参数的作用。在实验1中,WKY和SHR大鼠在静息时以及在脑室内(ICV)输注媒介物,催产素或催产素受体(OTR)拮抗剂期间的喷气应激后均记录了平均动脉压(MABP)和心率(HR) 。在实验2中,在事先给予V1a血管加压素受体(V1aR)拮抗剂后,在WKY大鼠中确定了载体,催产素和OTR拮抗剂的作用。在WKY或SHR大鼠中,静息MABP和HR均不受任何ICV输注的影响。在对照实验(车辆)中,SHR的升压对压力的反应明显更高。催产素增强了WKY大鼠的压力应激反应,但降低了SHR。在V1aR阻滞过程中,输注催产素完全消除了WKY大鼠对压力的升压反应。与输注V1a拮抗剂和赋形剂相比,V1aR和OTR的联合阻断引起的MABP对压力的反应明显更大。这项研究揭示了在警告压力期间,WKY和SHR大鼠的血压调节存在显着差异。具体而言,外源性催产素在WKY大鼠中对压力的压力反应增强是由其与V1aR相互作用引起的,内源性催产素通过同时与OTR和V1aR相互作用调节WKY大鼠在压力下的压力反应幅度。

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