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Role of vasopressin V1 antagonist in the action of vasopressin on the cooling-evoked hemodynamic perturbations of rats
Neuropeptides ( IF 2.5 ) Pub Date : 2019-08-01 , DOI: 10.1016/j.npep.2019.101939
Yung-Nien Yang , Hsien-Lung Tsai , Yu-Chieh Lin , Yia-Ping Liu , Che-Se Tung

We aimed to investigate the role of arginine vasopressin (AVP) acting via the AVPV1 receptor in the autonomic cardiovascular responses to cold stress (CS). The study was conducted on adult male Sprague-Dawley rats with telemetry transmitters implanted to monitor heart rate (HR) and systolic blood pressure (SBP) throughout the experiment course. Rats were divided into four groups and were given, respectively, saline (control group), AVPV1 antagonist (V1880) alone, and V1880 following the removal of sympathetic outflows using hexamethonium (HEX+V1880) or guanethidine (GUA + V1880). Rats were subjected to the CS stimuli (rapid immersion of the rat's limbs into 4 °C water). Hemodynamic responses were recorded at baseline (PreCS), during CS, and after CS. Data analysis was performed using descriptive methods and spectral and cross-spectral analysis of blood pressure variability (BPV) and heart rate variability (HRV). Key results showed that at PreCS, inhibition of AVPV1 increases SBP and HR as well as very-low-frequency BPV and low-frequency BPV, which is attenuated by hexamethonium (effect on SBP only) and guanethidine (effect on both SBP and HR). HEX+V1880 results in increased high-frequency BPV and attenuated very-low-frequency HRV, while GUA + V1880 results in increased high-frequency HRV and attenuated very-low-frequency HRV. During CS, we observed that SBP and HR, as well as very-low-frequency BPV and low-frequency BPV, were similar in the control group and the group with AVPV1 inhibition, while AVPV1 inhibition results in attenuated high-frequency BPV. Furthermore, we observed that changes produced by AVPV1 inhibition alone were affected differently by HEX+V1880 and GUA + V1880, particularly in low-frequency HRV and very-low-frequency HRV. The results support that AVPV1 mediates autonomic cardiovascular responses at both baseline and CS stimuli conditions are associated with central mechanism engagement.

中文翻译:

加压素V1拮抗剂在加压素对大鼠冷诱发血流动力学扰动的作用中的作用

我们旨在研究精氨酸加压素 (AVP) 在对冷应激 (CS) 的自主心血管反应中通过 AVPV1 受体起作用的作用。该研究是在成年雄性 Sprague-Dawley 大鼠身上进行的,这些大鼠植入了遥测发射器,以在整个实验过程中监测心率 (HR) 和收缩压 (SBP)。将大鼠分为四组,分别给予生理盐水(对照组)、单独的 AVPV1 拮抗剂(V1880)和使用六甲铵(HEX+V1880)或胍乙啶(GUA+V1880)去除交感神经流出物后的 V1880。大鼠接受 CS 刺激(将大鼠的四肢快速浸入 4°C 的水中)。在基线 (PreCS)、CS 期间和 CS 后记录血流动力学反应。使用描述性方法以及血压变异性 (BPV) 和心率变异性 (HRV) 的光谱和交叉光谱分析进行数据分析。关键结果表明,在 PreCS 中,抑制 AVPV1 会增加 SBP 和 HR 以及极低频 BPV 和低频 BPV,而六甲铵(仅对 SBP 有影响)和胍乙啶(对 SBP 和 HR 都有影响)会减弱这种作用. HEX+V1880 导致高频 BPV 增加并减弱极低频 HRV,而 GUA + V1880 导致高频 HRV 增加并减弱极低频 HRV。在CS期间,我们观察到SBP和HR以及极低频BPV和低频BPV在对照组和AVPV1抑制组中相似,而AVPV1抑制导致高频BPV减弱。此外,我们观察到,单独抑制 AVPV1 产生的变化受 HEX+V1880 和 GUA + V1880 的影响不同,特别是在低频 HRV 和极低频 HRV 中。结果支持 AVPV1 在基线和 CS 刺激条件下介导自主心血管反应与中枢机制的参与有关。
更新日期:2019-08-01
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