首页> 外文期刊>The Journal of Pharmacology and Experimental Therapeutics: Official Publication of the American Society for Pharmacology and Experimental Therapeutics >A Comparison between the Cardiovascular Actions of Urocortin 1 and Urocortin 2 (Stresscopin-Related Peptide) in Conscious Rats
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A Comparison between the Cardiovascular Actions of Urocortin 1 and Urocortin 2 (Stresscopin-Related Peptide) in Conscious Rats

机译:知觉大鼠中乌罗考丁1和乌罗考丁2(与骨甾醇相关的肽)的心血管作用的比较

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摘要

The aims of the study were,in conscious Sprague-Dawley rats,to compare the effects of stresscopin-related peptide (SRP) and urocortin (UCN) 1 on blood pressure,heart rate,and regional hemodynamics;to determine whether or not there were residual tachycardic effects of SRP or UCN1 after cardiac autonomic blockade;and to investigate a possible involvement of corticotropin releasing factor type 1 (CRF-,) receptor-mediated histamine release in the vasodilator actions of UCN1.SRP and UCN1 (both at 3 nmol/kg i.v.) caused hypotension,tachycardia,and mesenteric and hindquarters vasodilatation,but the magnitude and/or duration of the effects of UCN1 were generally greater than those of SRP.Pretreatment with atropine plus propranolol abolished the tachycardic effects of SRP and UCN1,and,under those conditions,the hypotensive effect of SRP,but not that of UCN1,was enhanced,probably because the hindquarters vasodilator effect of the latter was also reduced.Pretreatment with mepyramine plus cimetidine had no effect on the hemodynamic actions of either SRP or UCN1.It is concluded that,in conscious rats,the tachycardic effects of SRP and UCN1 are due to autonomic nervous activation mainly through baroreflex mechanisms.There is no evidence for an involvement of CRF1 receptor-mediated histamine release in the vasodilator actions of UCN1,but a propranolol-sensitive hindquarters vasodilator action of UCN,but not of SRP,was identified.
机译:该研究的目的是在有意识的Sprague-Dawley大鼠中比较应激铜相关肽(SRP)和尿皮质素(UCN)1对血压,心率和局部血流动力学的影响;确定是否存在心脏自主神经阻滞后SRP或UCN1的残留心动过速作用;并研究促肾上腺皮质激素释放因子1型(CRF-)受体介导的组胺释放可能参与UCN1.SRP和UCN1的血管舒张作用(均为3 nmol / kg iv)引起低血压,心动过速以及肠系膜和后肢血管舒张,但UCN1作用的幅度和/或持续时间通常大于SRP。阿托品+普萘洛尔预处理可消除SRP和UCN1的心动过速作用,并且,在这种情况下,SRP的降压作用增强,但UCN1的降压作用并未增强,这可能是因为后者的后肢血管舒张作用也降低了。美吡拉敏联合西咪地丁预处理结论:在有意识的大鼠中,SRP和UCN1的心动过速作用主要是由自主神经激活引起,主要是通过压力反射机制引起的。没有证据表明CRF1参与其中。受体介导的组胺在UCN1的血管舒张作用中释放,但对心得安的普萘洛尔敏感的后肢血管舒张作用,但未发现SRP。

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